2024-03-28T11:45:41Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/220832018-09-05T10:49:52Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Sanz-García, Marta
author
Valbuena, A.
author
López-Sánchez, Inmaculada
author
Blanco, Sandra
author
Fernández, Isabel F.
author
Vázquez-Cedeira, Marta
author
Lazo, Pedro A.
2010-03-08T17:20:25Z
2010-03-08T17:20:25Z
2010-03-08T17:20:25Z
Emerging Signaling Pathways in Tumor Biology : 135-156 (2010)
978-81-7895-477-6
http://hdl.handle.net/10261/22083
VRK (vaccinia-related kinase) is a group of three proteins in the human kinome. These proteins, mainly VRK1 and VRK2, have been studied in the context of their substrates and interacting proteins in order to identify and characterize their signaling pathway, as well as their effect on other signaling pathways. VRK1 is mostly a nuclear kinase that specifically phosphorylates p53, c-Jun, ATF2, CREB, BAF and histone H3. VRK1 is an early response gene and is implicated in regulation of cell cycle progression. VRK1 is activated in response to DNA damage phosphorylating p53, which is stabilized and activated; this
active p53 induces a downregulatory mechanism of VRK1 that permits the reversal of p53 induced effects. The activity of nuclear VRK1 is regulated by its interaction with the Ran small GTPase. Also, VRK1 is a downstream component of the signaling pathway of MEK-Plk3 that induces Golgi fragmentation in mitosis. VRK2 has two isoforms; VRK2A is cytosolic and bound to endoplasmic reticulum and mitochondrial membranes. VRK2B is a shorter isoform free in cytosol and nucleus.
VRK2A affects cellular signaling by interaction with scaffold proteins, as JIP1. The JIP1-VRK2A signalosome blocks the incorporation of JNK, preventing its activation,and thus reducing the stress response to inflammatory cytokines as interleukin-1β and
to hypoxia.
eng
openAccess
VRK
Kinases
Cell signalling
Cancer
Tumor
Vaccinia-related kinase (VRK) signaling
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/22083/1/7%20Lazo.pdf
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7 Lazo.pdf
URL
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text/plain
7 Lazo.pdf.txt
oai:digital.csic.es:10261/310612018-09-05T10:46:37Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Lazo, Pedro A.
2011-01-10T16:21:32Z
2011-01-10T16:21:32Z
2010
978-81-7895-477-6
http://hdl.handle.net/10261/31061
eng
openAccess
Emerging signaling pathways in tumor biology
libro
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
URL
https://digital.csic.es/bitstream/10261/31061/1/lazo%20book.pdf
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URL
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File
MD5
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lazo book.pdf.txt
oai:digital.csic.es:10261/595632016-02-17T12:52:29Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
San Miguel, Jesús F.
author
Mateos, Maria Victoria
2012-11-06T12:20:08Z
2012-11-06T12:20:08Z
2011
Bortezomib in the Treatment of Multiple Myeloma VII: 53- 68 (2011)
http://hdl.handle.net/10261/59563
10.1007/978-3-7643-8948-2_4
Although multiple myeloma (MM) remains a disease that is incurable with conventional treatments, important changes have recently been introduced in the management of the disease as a result of advances in our knowledge of its pathogenesis and the availability of novel agents. Bortezomib is a first-in-class proteasome inhibitor that targets not only the MM cell but also its interaction with the bone marrow microenvironment. It represents an excellent example of a novel class of agents that have quickly moved from the bench to the bedside. Four randomised trials have evaluated the role of bortezomib-based combinations as an induction therapy in transplant candidate myeloma patients, revealing a high efficacy (>80% response rate, with 20-30% complete response (CR)) that increased after autologous stem cell transplant, confirming the results of numerous pilot studies of various bortezomib-based combinations. In patients who are not candidates for transplant, bortezomib in combination with melphalan and prednisone has also proved to be superior to conventional therapy, with high overall and CR rates and a significantly longer time to progression and overall survival. Moreover, new strategies are being explored in patients who are not candidates for transplant based on the optimisation of the VISTA schedule and using weekly doses of bortezomib to improve tolerability. Overall, these results have established bortezomib-based combinations as key treatment options for newly diagnosed myeloma patients. © Springer Basel AG 2011.
eng
closedAccess
Bortezomib in the upfront treatment of multiple Myeloma
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/59563/1/accesoRestringido.pdf
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accesoRestringido.pdf.txt
oai:digital.csic.es:10261/605812016-02-17T13:00:02Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Sánchez-Muñoz, Laura
author
Teodosio, Cristina
author
Escribano, Luis
2012-11-19T14:19:32Z
2012-11-19T14:19:32Z
2011
Methods in Cell Biology 103(Cap. 14): 333-359 (2011)
http://hdl.handle.net/10261/60581
10.1016/B978-0-12-385493-3.00014-0
Mastocytosis is a term used to designate a heterogeneous group of disorders characterized by an abnormal proliferation and accumulation of mast cells (MCs) in one or multiple tissues including skin, bone marrow (BM), liver, spleen, and lymph nodes, among others.Recent advances in our understanding of mast cell biology and disease resulted in the identification of important differences in the expression of mast cell surface antigens between normal and neoplastic mast cells. Most notably, detection of aberrant expression of CD25 and CD2 on the surface of neoplastic mast cells but not on their normal counterparts lead to the inclusion of this immunophenotypic abnormality in the World Health Organization diagnostic criteria for systemic mastocytosis. Aberrant mast cell surface marker expression can be detected in the bone marrow aspirate by flow cytometry, even in patients lacking histopathologically detectable aggregates of mast cells in bone marrow biopsy sections. These aberrant immunophenotypic features are of great relevance for the assessment of tissue involvement in mastocytosis with consequences in the diagnosis, classification, and follow-up of the disease and in its differential diagnosis with other entities.In this chapter, we provide the reader with information for the objective and reproducible identification of pathologic MCs by using quantitative multiparametric flow cytometry, for their phenotypic characterization, and the criteria currently used for correct interpretation of the immunophenotypic results obtained. © 2011 Elsevier Inc.
eng
closedAccess
Immunophenotypic Characterization of Bone Marrow Mast Cells in Mastocytosis and Other Mast Cell Disorders
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/60581/1/accesoRestringido.pdf
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accesoRestringido.pdf.txt
oai:digital.csic.es:10261/614332016-02-17T10:40:46Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Pérez-Hidalgo, Livia
author
Moreno, Sergio
author
Martín-Castellanos, Cristina
2012-11-28T12:43:31Z
2012-11-28T12:43:31Z
2008
Recombination and Meiosis: 307-353 (2008)
http://hdl.handle.net/10261/61433
The study of meiosis regulation has always been carried out in parallel with mitotic cell cycle discoveries. The basic cell cycle machinery that regulates mitosis, based on fluctuations in the activity of cyclin-dependent kinases (CDKs), is responsible for the main transitions that occur during meiosis. However, the special characteristics of meiosis (e.g., the absence of an S-phase between meiosis I and meiosi II, a long prophase in which homologous recombination events occur, etc.) require specific regulation, and cells respond to this challenging situation in different ways. In some cases, mitotic regulators carry out the new functions or change their relative importance in a particular process, while in other cases novel meiosis-specific regulators emerge. In this chapter, we shall analyze these special modifications, beginning with the specific signals that cells receive to exit the mitotic cell cycle and enter meiosis. We shall review how mitotic regulators adapt to the necessities of the meiotic program, paying particular attention to meiosis-specific factors whose functions are essential for meiosis to be completed successfully.
eng
closedAccess
Modified cell cycle regulation in meiosis
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/61433/1/accesoRestringido.pdf
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accesoRestringido.pdf.txt
oai:digital.csic.es:10261/630612021-11-22T12:54:34Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Dosil, Mercedes
2012-12-17T13:10:20Z
2012-12-17T13:10:20Z
2010
Methods in Enzymology 485: 329-348 (2010)
http://hdl.handle.net/10261/63061
10.1016/B978-0-12-381296-4.00019-1
21050926
Mating pheromone receptors of the yeast Saccharomyces cerevisiae are useful models for the study of G protein-coupled receptors. The mating pheromone receptors, Ste2 and Ste3, are not essential for viability so they can be readily targeted for analysis by a variety of genetic approaches. This chapter will describe methods for identification of two kinds of mutants that have been very informative about the mechanisms of receptor signaling: constitutively active mutants and dominant-negative mutants. Interestingly, these distinct types of mutants have revealed complementary information. Constitutive signaling is caused by mutations that are thought to weaken interactions between the seven transmembrane domains (TMDs), whereas the dominant-negative mutants apparently stabilize contacts between TMDs and lock receptors in the off conformation. In support of these conclusions, certain combinations of constitutively active and dominant-negative mutants restore nearly normal signaling properties. © 2010 Elsevier Inc.
eng
closedAccess
Strategies for isolating constitutively active and dominant-negative pheromone receptor mutants in yeast
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/63061/1/accesoRestringido.pdf
File
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accesoRestringido.pdf
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accesoRestringido.pdf.txt
oai:digital.csic.es:10261/827502020-09-30T12:12:06Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Mollinedo, Faustino
author
Gajate, Consuelo
funder
Ministerio de Ciencia e Innovación (España)
funder
European Commission
funder
Red Temática de Investigación Cooperativa en Cáncer (España)
funder
Instituto de Salud Carlos III
funder
Junta de Castilla y León
funder
Instituto de Salud Carlos III
2013-09-25T09:06:08Z
2013-09-25T09:06:08Z
2012
A Toxicological /Pharmacological Approach to Chemico-Biological Interactions at a Membrane Level: 27-40 (2012)
http://hdl.handle.net/10261/82750
http://dx.doi.org/10.13039/501100004837http://dx.doi.org/10.13039/501100000780http://dx.doi.org/10.13039/501100004587http://dx.doi.org/10.13039/501100014180
The dynamic nature of membrane along with an uneven distribution of lipids leads to the formation of specialized membrane domains where proteins can selectively be included or excluded. In this regard, the dynamic and preferential clustering and packing of sphingolipids and cholesterol into moving platforms, named as lipid rafts, form membrane domains that act as scaffolds for the attachment of specific proteins and for the proper functioning of a number of signaling cascades. Lipid rafts harbor several signaling routes that promote cell survival and proliferation, and thereby they could play a role in the development of cancer. On the other hand, evidences in the last decade have shown that lipid rafts can also serve as organizing centers for the assembly of apoptotic and signaling molecules involved in cell death, thus opening a new avenue in cancer therapy. Recruitment of death receptors and downstream apoptotic signaling molecules in aggregated lipid rafts has led to the emerging concept of a plasma membrane platform designated as “cluster of apoptotic signaling molecule-enriched rafts” (CASMER) that may play a role in the regulation of apoptosis. In addition, lipid rafts also play a major role in neurotoxicity, including the production and aggregation of amyloid-β peptide (Aβ) to form neurotoxic Aβ oligomers in the brain, which are widely believed to drive Alzheimer’s disease pathology. Alterations in cholesterol have been detected in cell models for cancer and neurodegenerative diseases, which might lead to changes in cholesterol-rich rafts and thereby in the regulation of cell death or survival. However, it is currently unclear what the potential mechanisms underlying cholesterol perturbations are. Growing evidence suggests that compartmentalization of macrocomplexes and signaling routes in lipid rafts has a crucial role in the regulation of cell fate, being of major importance in different pathologies, including cancer and neurodegenerative diseases. Despite the underlying mechanisms and functional impact of protein compartmentalization are still not well understood, the modulation of lipid rafts opens new approaches in the treatment of these diseases for which current available therapies are not satisfactory.
eng
openAccess
Lipid rafts, cholesterol and apoptosis in cancer and neurodegenerative diseases
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/82750/1/Lipid%20rafts.pdf
File
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Lipid rafts.pdf
URL
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Lipid rafts.pdf.txt
oai:digital.csic.es:10261/1232352018-09-12T12:18:44Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Dasilva, Noelia
author
González González, María
author
Díez, Paula
author
Jara-Acevedo, Ricardo
author
Lourido, Lucía
author
Sayagués, José María
author
Orfao, Alberto
author
Fuentes, Manuel
2015-10-09T10:21:23Z
2015-10-09T10:21:23Z
2014
Comprehensive Analytical Chemistry 63(Cap.6): 137-157 (2014)
http://hdl.handle.net/10261/123235
10.1016/B978-0-444-62651-6.00006-4
Biomarker discovery has been increased by proteomics approached in high-throughput format coupled with novel nanotechniques, which can be classified in label-based and label-free detection systems. In this chapter, the application of these novel approaches in biomarker discovery is reviewed, indicating their advantages and disadvantages, challenges and implications, in addition to the improvement of sensitivity and selectivity by using nanoproteomics approaches.
eng
closedAccess
Emerging nanotechniques in proteomics
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/123235/1/accesoRestringido.pdf
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accesoRestringido.pdf.txt
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oai:digital.csic.es:10261/1232442018-09-04T12:17:29Zcom_10261_112com_10261_1com_10261_25col_10261_1247col_10261_908
DIGITAL.CSIC
author
Casado-Vela, Juan
author
Fuentes, Manuel
author
Franco-Zorrilla, José Manuel
funder
Ministerio de Economía y Competitividad (España)
funder
European Commission
funder
Consejo Superior de Investigaciones Científicas (España)
2015-10-09T11:30:06Z
2015-10-09T11:30:06Z
2014
Advances in Protein Chemistry and Structural Biology 95(Cap.8): 231-281 (2014)
http://hdl.handle.net/10261/123244
10.1016/B978-0-12-800453-1.00008-7
http://dx.doi.org/10.13039/501100003329http://dx.doi.org/10.13039/501100000780http://dx.doi.org/10.13039/501100003339
In this report, we focus on two different array-based technologies that enable large-scale screening of protein interactions. First, protein arrays focus on the identification of protein-protein interactions (PPIs). Second, DNA arrays have also evolved to explore the identification of protein-DNA interactions (PDIs), offering novel tools to control key biological processes. Such a tool is termed protein-binding DNA arrays (also protein-DNA arrays or protein-binding microarrays). These two array-based technologies share unrivaled screening capabilities and constitute valid approaches to address biological questions at the molecular level and, eventually, may be used in biomedical applications. Outstanding achievements of these technologies and their eventual application in biomedicine are discussed here, including the identification and characterization of biomarkers, screening of PPIs, detection of protein posttranslational modifications and biofluid profiling. Advantages and limitations of protein arrays, protein-binding arrays, and other proteomic technologies are also discussed here. Finally, we built a list of dedicated databases and on-line resources comprising updated information on human PPIs and PDIs that can serve as a toolbox for researchers in the field. © 2014 Elsevier Inc.
eng
closedAccess
Screening of protein-protein and protein-DNA interactions using microarrays: Applications in biomedicine
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/123244/1/accesoRestringido.pdf
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accesoRestringido.pdf.txt
URL
https://digital.csic.es/bitstream/10261/123244/5/accesoRestringido.pdf.txt
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accesoRestringido.pdf.txt
oai:digital.csic.es:10261/1341752018-09-27T06:49:28Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
De Las Rivas, Javier
author
Prieto-Sánchez, Carlos
2016-06-28T12:43:01Z
2016-06-28T12:43:01Z
2012
Bioinformatics and Drug Discovery: 279-296 (2012)
http://hdl.handle.net/10261/134175
10.1007/978-1-61779-965-5_12
Proteins are biomolecular structures that build the microscopic working machinery of any living system. Proteins within the cells and biological systems do not act alone, but rather team up into macromolecular structures enclosing intricate physicochemical dynamic connections to undertake biological functions. A critical step towards unraveling the complex molecular relationships in living systems is the mapping of protein-to-protein physical >interactions>. The complete map of protein interactions that can occur in a living organism is called the >interactome>. Achieving an adequate atlas of all the protein interactions within a living system should allow to build its interaction network and to identity the >central nodes> that can be critical for the function, the homeostasis, and the movement of such system. Focusing on human studies, the data about the human interactome are most relevant for current biomedical research, because it is clear that the location of the proteins in the interactome network will allow to evaluate their centrality and to redefine the potential value of each protein as a drug target. This chapter presents our current knowledge on the human protein-protein interactome and explains how such knowledge can help us to select adequate targets for drugs.
eng
closedAccess
Protein interactions: Mapping interactome networks to support drug target discovery and selection
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/134175/1/accesoRestringido.pdf
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accesoRestringido.pdf
oai:digital.csic.es:10261/1344092018-09-05T09:39:07Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Robledo, Cristina
author
García, Juan L.
author
Hernández, Jesús M.
funder
Instituto de Salud Carlos III
funder
Ministerio de Ciencia e Innovación (España)
funder
Instituto de Salud Carlos III
funder
Red Temática de Investigación Cooperativa en Cáncer (España)
funder
Fundación Caja de Burgos
funder
Junta de Castilla y León
funder
Universidad de Salamanca
2016-07-05T06:59:44Z
2016-07-05T06:59:44Z
2013
Array Comparative Genomic Hybridization: 121-145 (2013)
http://hdl.handle.net/10261/134409
10.1007/978-1-62703-281-0_8
http://dx.doi.org/10.13039/501100004587http://dx.doi.org/10.13039/501100004837http://dx.doi.org/10.13039/501100014180
BAC array-CGH is a powerful method to identify DNA copy number changes (gains, amplifications and deletions) on a genome-wide scale, and to map these changes to genomic sequence. It is based on the analysis of genomic DNA isolated from test and reference cell populations, the differential labelling with fluorescent dyes and the co-hybridization with a genomic array. BAC array-CGH has proven to be a specific, sensitive, and reliable technique, with considerable advantages compared to other methods used for the analysis of DNA copy number changes. The application of genome scanning technologies and the recent advances in bioinformatics tools that enable us to perform a robust and highly sensitive analysis of array-CGH data, useful not only for genome scanning of tumor cells but also in the identification of novel cancer related genes, oncogenes and suppressor genes. Cytogenetic analysis provides essential information for diagnosis and prognosis in patients with hematologic malignancies such as lymphomas. However, the chromosomal interpretation in non-Hodgkin lymphoma (NHL) is sometimes inconclusive. Copy number aberrations identified by BAC array-CGH analyses could be a complementary methodology to chromosomal analysis. In NHL the genomic imbalances might have a prognostic rather than a diagnostic value. In fact, the diagnosis of NHL is based on pathological and molecular cytogenetics data. Furthermore genetic variations and their association with specific types of lymphoma development, and elucidation of the variable genetic pathways leading to lymphoma development, are important directions for future cancer research. Array-CGH, along with FISH and PCR, will be used for routine diagnostic purposes in near future.
eng
closedAccess
MegaCHOP
Diffuse large B-cell lymphoma
BAC (bacterial artificial chromosome) clone
Non-Hodgkin lymphoma
BAC array-CGH
Clinical applications of BAC array-CGH to the study of diffuse large B-cell lymphomas
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/134409/1/accesoRestringido.pdf
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accesoRestringido.pdf
oai:digital.csic.es:10261/1346622018-09-27T06:38:26Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
De Las Rivas, Javier
author
Aibar, Sara
author
Rosón, Beatriz
2016-07-11T10:38:17Z
2016-07-11T10:38:17Z
2014
Comprehensive Analytical Chemistry 63: 355-384 (2014)
http://hdl.handle.net/10261/134662
10.1016/B978-0-444-62651-6.00016-7
Current genome-wide studies of gene expression are achieved using two major omic technologies: high-density oligonucleotide microarrays and deep RNA sequencing. These high-throughput experimental techniques allow the detection of most known genes and are providing global gene expression profiles and gene signatures for normal and pathological states of multiple biological systems, including many human samples and cell types. At present, microarrays technology is still better established and more widely used than RNA sequencing and has provided the most gene expression data. Most analyses of the human transcriptome focus on the identification and characterization of protein-coding genes; however, the complexity of the human transcriptomic system has been found to be much more than expected, and we still do not have a clear genome-wide compendium of the genes that are active in each human tissue and cell type. Development and application of adequate bioinformatic methods is the only way to achieve a proper use of the omic-wide gene expression datasets. Thorough analysis and integration of omic studies is essential to achieve an unbiased global characterization of the active human transcriptome. In this chapter we present and describe several important concepts in modern transcriptomics and bioinformatic methods to analyze genome-wide data mainly derived from microarrays technology but also from deep-sequencing technology, in both cases applied to gene expression measurements.
eng
closedAccess
Microarray
Next-generation sequencing
Bioinformatics
Gene expression analysis
Gene expression analysis and profiling of microarrays data and RNA-sequencing data
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/134662/1/accesoRestringido.pdf
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application/pdf
accesoRestringido.pdf
oai:digital.csic.es:10261/1360132018-09-05T10:49:52Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Lazo, Pedro A.
author
Lozano, José
2016-08-29T11:02:55Z
2016-08-29T11:02:55Z
2012
Encyclopedia of Cancer: 1-5 (2012)
http://hdl.handle.net/10261/136013
10.1007/978-3-642-27841-9_5164-10
An individual cell has over one billion proteins, of which ten percent form part of signaling pathways and networks, and none of them is exclusive for a single pathway. Thus, pathway components need to be partially preorganized so that signal transduction is not limited by the diffusion kinetics of individual molecules. These molecules need to be organized into complexes that will affect timing, location, and even specificity and magnitude of a single response, such as to growth factors or protection against DNA damage, for example. Thus, there is a cellular need to organize pathways both in time and space, a role that is achieved by scaffold proteins.
eng
closedAccess
Scaffold proteins
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/136013/1/accesoRestringido.pdf
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oai:digital.csic.es:10261/1360152018-09-05T10:49:52Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Valbuena, A.
author
Sanz-García, Marta
author
López-Sánchez, Inmaculada
author
Vega, Francisco M.
author
Sevilla Hernández, Ana
author
Lazo, Pedro A.
2016-08-29T11:14:30Z
2016-08-29T11:14:30Z
2012
Encyclopedia of Signalling Molecules: 1992-1996 (2012)
http://hdl.handle.net/10261/136015
10.1007/978-1-4419-0461-4_561
VRK1 is a Ser-Thr kinase functionally associated with entry in cell cycle, and is required for nuclear envelope dynamics, chromatin condensation, and Golgi fragmentation.
VRK1 is mostly located in the nucleus and in the Golgi apparatus. Among its substrates are several transcription factors: p53, c-Jun, ATF2, and CREB1. VRK1 probably acts cooperating with other signaling pathways that also phosphorylate these transcription factors. VRK1 stabilizes p53 by a specific phosphorylation in Thr18 and after induction of p53 responses, there is a VRK1 downregulation in the lysosome and in which the autophagic pathway participates in a p53-dependent manner. VRK1 contributes to chromatin condensation and nuclear envelop kinetics by phosphorylation of histone H3 and BAF. VRK1 is downstream of MEK1 and Plk3 in the pathway inducing Golgi fragmentation during mitosis. VRK1 is expressed in most tissues, is necessary in the early G1 phase for entry in cell cycle, and is associated with proliferation markers (Klerkx et al. 2009).
eng
closedAccess
Vaccinia virus B1R-related kinase 1
VRK-1
Vaccinia-related kinase 1
VRK1
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/136015/1/accesoRestringido.pdf
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oai:digital.csic.es:10261/1360172018-09-05T10:49:52Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Blanco, Sandra
author
Fernández, Isabel F.
author
Vázquez-Cedeira, Marta
author
Monsalve, Diana M.
author
Merced, Triana
author
Lazo, Pedro A.
2016-08-29T11:18:49Z
2016-08-29T11:18:49Z
2012
Encyclopedia of Signalling Molecules: 1996-2000 (2012)
http://hdl.handle.net/10261/136017
10.1007/978-1-4419-0461-4_562
VRK2 is a Ser-Thr kinase and has two isoforms, cytosolic and nuclear. The full-length VRK2 cytosolic isoform (A) inhibits MAPK signaling by a direct interaction with the corresponding JIP1 or KSR1 scaffold proteins. As a consequence, high levels of VRK2A inhibit in a dose-dependent manner signals mediated by the TAK1-MKK7-JNK in response to hypoxia or interleukin, and the signal of the ERBB2-RAS-RAF-MEK-ERK pathway. Downregulation of VRK2A relieves this inhibition and allows signal transmission in response to stimuli initiated in receptor-tyrosine kinases (RTK), such as ERBB2. Thus, in breast cancer VRK2A and ERBB2 present an inverse correlation.
eng
closedAccess
Vaccinia virus B1R-related kinase 2
VRK-2
Vaccinia-related kinase 2
VRK2
capítulo de libro
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URL
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accesoRestringido.pdf
oai:digital.csic.es:10261/1360202018-09-05T10:49:53Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Vázquez-Cedeira, Marta
author
Monsalve, Diana M.
author
Sanz-García, Marta
author
Lazo, Pedro A.
2016-08-29T11:26:38Z
2016-08-29T11:26:38Z
2012
Encyclopedia of Signalling Molecules: 1955-1957 (2012)
http://hdl.handle.net/10261/136020
10.1007/978-1-4419-0461-4_101469
VRK3 is the most divergent member of the VRK family. It has no kinase activity due to several substitutions in key residues within its catalytic domain. VRK3 is mostly located within the nucleus and appears to play a scaffold role, where it downregulates MAPK
signaling and reduces the level of p-ERK by recruiting the VHR phosphatase
eng
closedAccess
VRK3
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/136020/1/accesoRestringido.pdf
File
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application/pdf
accesoRestringido.pdf
oai:digital.csic.es:10261/1360212018-09-05T10:46:37Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Lazo, Pedro A.
author
Barcia, R.
2016-08-29T11:30:39Z
2016-08-29T11:30:39Z
2012
Encyclopedia of Signalling Molecules: 343-347 (2012)
http://hdl.handle.net/10261/136021
10.1007/978-1-4419-0461-4_566
CD53 is one of the least characterized members of the tetraspanin family. CD53 is integrated in the tetraspanin web, and sends intracellular signals, directly or indirectly via PKC, AKT, and γ-glutamyl transpeptidase (GGT). Its expression can affect cell survival, resistance to apoptosis, and radiation sensitivity. In B-cell development CD53 is a marker of mature B cells. In human B-cell malignancies, the pattern of tetraspanin expression identifies the developmental stage of the corresponding tumors. The pattern of tetraspanins can be used to differentiate B-cell malignancies in an individual patient with several lymphoid tumors.
eng
closedAccess
Ox-44
OX44
MOX44
Tspan25l
Cell surface glycoprotein CD53
CD53 antigen
Tetraspanin-25
Tspan-25
Leukocyte surface antigen CD53
CD53
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/136021/1/accesoRestringido.pdf
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15753
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accesoRestringido.pdf
oai:digital.csic.es:10261/1360232018-09-12T11:33:40Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Cobaleda, César
author
Vicente-Dueñas, Carolina
author
Romero-Camarero, Isabel
author
Sánchez García, Isidro
2016-08-29T11:39:10Z
2016-08-29T11:39:10Z
2012
Encyclopaedia of Life Sciences: (2012)
http://hdl.handle.net/10261/136023
10.1002/9780470015902.a0020860.pub2
Cancer stem cells (CSCs) are the pathological counterpart of normal somatic tissue stem cells. They possess the capacities to self-renew and to generate a more differentiated, rapidly dividing and expanding tumour progeny. Although they constitute just a small percentage of the tumour mass, they are responsible for its maintenance and, therefore, they should be the target of anticancer treatments. The existence of CSCs is still a matter of controversy for certain tumour types – some of which are actually frequent and clinically relevant – but it is confirmed in many others. Moreover, CSCs are predictably genetically diverse, and their frequency and phenotype can vary in the course of the disease. However, CSCs have nowadays been identified in almost all the frequent types of tumours, and recent findings have shown that CSC gene expression signatures can be predictive of adverse clinical outcome, therefore maintaining the study of CSCs at the forefront of cancer research.
eng
closedAccess
Cancer
Mouse models
Leukaemia
Solid tumours
Stem cells
Cancer stem cells
capítulo de libro
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URL
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oai:digital.csic.es:10261/1360252020-05-25T14:11:08Zcom_10261_79com_10261_1com_10261_112col_10261_1214col_10261_1247
DIGITAL.CSIC
author
Vicente-Dueñas, Carolina
author
Campos-Sánchez, Elena
author
Hourcade, Juan M.
author
Romero-Camarero, Isabel
author
Sánchez García, Isidro
author
Cobaleda, César
2016-08-29T11:47:31Z
2016-08-29T11:47:31Z
2013
Stem Cells and Cancer Stem Cells 9(Cap.22): 227-234 (2013)
http://hdl.handle.net/10261/136025
10.1007/978-94-007-5645-8_22
The complexity of cancer biology cannot be understood in all its depth solely with the study of human patients and the samples derived from them. These types of studies are undeniably essential, but the heterogeneity among human patients, together with the long latency of the disease and its usually delayed diagnosis, make it difficult to recapitulate all the phases of the disease from human studies. In this context, genetically engineered mouse models (GEMMs) of human cancer are essential tools for our understanding of the processes leading to the disease. The sophistication of the techniques allowing us to model cancer in mice has increased enormously over the last years, to the extent that we can now induce, study and manipulate the disease, its evolution and its response to treatment in a way that is not possible in humans. The identification of cancer stem cells (CSCs) as the only cells within the tumor with the capacity of propagating and maintaining the disease has added a new layer of complexity to our understanding of cancer. However, most of GEMMs generated and characterized to date have not being designed to take into account the existence of CSCs and their role in the disease generation, evolution and response to treatment. In this chapter we briefly revise the major milestones in the history of the generation of mouse models of cancer, and propose new strategies for the future, taking into consideration what we nowadays know about the hierarchical nature of tumors.
eng
closedAccess
Cancer stem cells and modeling cancer in the mouse
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/136025/1/accesoRestringido.pdf
File
MD5
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accesoRestringido.pdf
oai:digital.csic.es:10261/1360282020-05-25T14:11:08Zcom_10261_112com_10261_1com_10261_79col_10261_1247col_10261_1214
DIGITAL.CSIC
author
Campos-Sánchez, Elena
author
Romero-Camarero, Isabel
author
Sánchez García, Isidro
author
Cobaleda, César
2016-08-29T11:59:43Z
2016-08-29T11:59:43Z
2013
Role of Cancer Stem Cells in Cancer Biology and Therapy: 167-198 (2013)
http://hdl.handle.net/10261/136028
After many years of struggle against the traditional theories, cancer stem cells (CSCs) are finally coming of age as the main responsible for the maintenance and relapse of human cancer. there are two main reasons for this fact. First, the enormous amount of quickly accumulating experimental evidences proving their existence and their contribution to cancer maintenance and survival in humans. Second, the patent e vidence of the very slow advance of our fight against cancer in the las 50 years. Indeed, althought early detection and screening programs have increased the chances of diagnosing cancer at very early stages, the prognosis for disseminated tumors is as dismal today as it was 5 decades ago. It is therefore clear that a new conceptual framework is required in our approach to treat cancer. The acknowledgement of the existence of CSCs provides this framework and opens new avenues for exploring therapeutic approaches. In this chapter we revise the most recent discoveries in the research aimed at the targeting and elimination of CSCs.
eng
closedAccess
Current concepts of how to eliminate cancer stem cells
capítulo de libro
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
URL
https://digital.csic.es/bitstream/10261/136028/1/accesoRestringido.pdf
File
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accesoRestringido.pdf
oai:digital.csic.es:10261/1360312018-09-12T11:33:40Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Iglesias, Juan Manuel
author
García-Ramírez, Idoia
author
Martín-Lorenzo, Alberto
author
Ruiz-Roca, Lucía
author
Sánchez García, Isidro
2016-08-29T12:18:04Z
2016-08-29T12:18:04Z
2014
Cancer Stem Cells: 61-77 (2014)
http://hdl.handle.net/10261/136031
10.1002/9781118356203.ch5
Several recent studies of the effect of oncogenes in stem cells in cancer development implicate that tumor reprogramming (where the maintenance of oncogene expression is not critical for the generation of differentiated tumor cells) might represent a potentially important mechanism of tumor development for many types of cancer and that, if this is the case, the oncogenes that initiate tumor formation might be dispensable for tumor progression and/or maintenance. The practical implications that this new point of view has for the therapy of cancer are obviously enormous. This chapter addresses the impact of these results toward a better understanding of carcinogenesis and proposes research avenues for tackling these issues in the future.
eng
closedAccess
Epithelial to mesenchymal transition (EMT)
Reprogramming-like disease
Pluripotency-related genes
Organ development
Mesenchymal to epithelial transition (MET)
Human cancer
Cancer stem cell (CSC) theory
Cancer stem cells as a result of a reprogramming-like mechanism: implications in tumor development and treatment
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/136031/1/accesoRestringido.pdf
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15753
application/pdf
accesoRestringido.pdf
oai:digital.csic.es:10261/1360332018-09-12T11:33:40Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Vicente-Dueñas, Carolina
author
Romero-Camarero, Isabel
author
Flores, Teresa
author
Cruz, Juan Jesús
author
Sánchez García, Isidro
funder
Ministerio de Ciencia e Innovación (España)
funder
European Commission
funder
Ministerio de Economía y Competitividad (España)
funder
Junta de Castilla y León
funder
Fundación Sandra Ibarra - Solidaridad Frente al Cáncer
funder
National Institutes of Health (US)
2016-08-29T12:45:01Z
2016-08-29T12:45:01Z
2011
Cancer Stem Cells Theories and Practice (Cap.4): 53-60 (2011)
978-953-307-225-8
http://hdl.handle.net/10261/136033
10.5772/13761
http://dx.doi.org/10.13039/501100004837http://dx.doi.org/10.13039/501100000780http://dx.doi.org/10.13039/501100003329http://dx.doi.org/10.13039/501100007649http://dx.doi.org/10.13039/100000002http://dx.doi.org/10.13039/501100014180
eng
openAccess
Cancer stem cells as a result of a reprogramming-like mechanism
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/136033/1/Like%20Mechanism.pdf
File
MD5
55780f6d141b555289c7e449e4e48287
257942
application/pdf
Like Mechanism.pdf
oai:digital.csic.es:10261/1360402018-09-12T11:33:41Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Vicente-Dueñas, Carolina
author
González-Herrero, Inés
author
García-Ramírez, Idoia
author
Sánchez García, Isidro
2016-08-30T06:53:33Z
2016-08-30T06:53:33Z
2014
Atlas of Genetics and Cytogenetics in Oncology and Haematology (2014)
http://hdl.handle.net/10261/136040
The MAFB protein is a basic leucine zipper (bZIP) transcription factor that plays important roles both in development and in the regulation of lineage-specific hematopoiesis. This gene contains no introns. The abnormal function of MAFB has been implicated in multiple myeloma, myeloid leukemias, multicentric carpotarsal osteolysis, Dupuytren's disease and nonsyndromic cleft lip.
eng
closedAccess
MAFB (v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog B)
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/136040/1/accesoRestringido.pdf
File
MD5
42637ae8545636bc41605c1740a9a84e
15753
application/pdf
accesoRestringido.pdf
oai:digital.csic.es:10261/1582042019-12-17T11:24:26Zcom_10261_112com_10261_1com_10261_39col_10261_1247col_10261_1174
DIGITAL.CSIC
author
Caloca, María J.
author
Barrio-Real, Laura
author
González-Sarmiento, Rogelio
2017-12-15T07:51:37Z
2017-12-15T07:51:37Z
2016
Neuropathology of Drug Addictions and Substance Misuse: 125-132 (2016)
http://hdl.handle.net/10261/158204
10.1016/B978-0-12-800213-1.00012-2
Tobacco addiction is a complex disorder that involves multiple molecular mechanisms and is influenced by genetic factors. Repeated exposure to nicotine induces the remodeling of synaptic connections, a process that contributes to the long-lasting nature of tobacco addiction. Rho GTPases are key regulators of synaptic structure and function and, therefore, these proteins have a potential role in nicotine addiction. In this chapter we will briefly describe some studies that identify genes encoding Rho GTPases and their regulators as candidate genes for smoking-related behaviors, with special focus on the CHN2 gene. The CHN2 gene encodes the β2-chimaerin, a member of the chimaerin family of GTPase activating proteins that selectively inactivates the GTPase Rac. Genetic studies suggest that nucleotide variants of the CHN2 gene may influence success in smoking cessation. In addition, work has identified a significant association of the rs186911567 polymorphism in the CHN2 gene with smoking in a Spanish population. We discuss how this polymorphism could alter β2-chimaerin function and the signaling pathways mediated by this protein that could influence smoking behavior.
eng
closedAccess
Smoking
Single nucleotide polymorphism
Rho GTPase
Nicotine addiction
GTPase activating protein
CHN2
Synaptic plasticity
β2-Chimaerin
Rho GTPases and their regulators in addiction: A focus on the association of a ß2-chimaerin polymorphism with smoking
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/158204/1/accesoRestringido.pdf
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accesoRestringido.pdf
oai:digital.csic.es:10261/1686892020-12-13T09:14:52Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Manso, José A.
author
García-Rubio, Inés
author
Gómez-Hernández, María
author
Ortega, Esther
author
Martínez Buey, Rubén
author
Carballido Vázquez, Ana M.
author
Carabias, Arturo
author
Alonso-García, Noelia
author
Pereda, José M. de
funder
European Commission
funder
Ministerio de Economía y Competitividad (España)
2018-08-14T09:37:25Z
2018-08-14T09:37:25Z
2016
Methods in Enzymology 569: 177-196 (2016)
978-0-12-803469-9
http://hdl.handle.net/10261/168689
10.1016/bs.mie.2015.05.002
http://dx.doi.org/10.13039/501100000780http://dx.doi.org/10.13039/501100003329
26778559
Plectin and BPAG1e belong to the plakin family of high-molecular-weight proteins that interconnect the cytoskeletal systems and anchor them to junctional complexes. Plectin and BPAG1e are prototypical plakins with a similar tripartite modular structure. The N- and C-terminal regions are built of multiple discrete structural domains, while the central rod domain mediates dimerization by coiled-coil interactions. Owing to the mosaic organization of plakins, the structure of their constituent individual domains or small multi-domain segments can be analyzed isolated. Yet, understanding the integrated function of large regions, oligomers, and heterocomplexes of plakins is difficult due to the large and segmented structure. Here, we describe methods for the production of plectin and BPAG1e samples suitable for structural and biophysical analysis. In addition, we discuss the combination of hybrid methods that yield information at several resolution levels to study the complex, multi-domain, and flexible structure of plakins.
eng
closedAccess
Recombinant expression
Spectrin repeat
Hybrid methods
DEER
SAXS
Crystallography
Protein structure
Plakin
Purification and structural analysis of plectin and BPAG1e
capítulo de libro
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
URL
https://digital.csic.es/bitstream/10261/168689/1/accesoRestringido.pdf
File
MD5
42637ae8545636bc41605c1740a9a84e
15753
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accesoRestringido.pdf
oai:digital.csic.es:10261/1686902020-12-13T09:18:21Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Díez, Paula
author
Fuentes, Manuel
funder
Instituto de Salud Carlos III
funder
Fundación Memoria de D. Samuel Solorzano Barruso
funder
European Commission
funder
Junta de Castilla y León
2018-08-14T09:43:45Z
2018-08-14T09:43:45Z
2016
Proteogenomics: 153-162 (2016)
http://hdl.handle.net/10261/168690
10.1007/978-3-319-42316-6_10
http://dx.doi.org/10.13039/501100004587http://dx.doi.org/10.13039/501100000780http://dx.doi.org/10.13039/501100014180
27686811
The vast repertoire of immunoglobulins produced by the immune system is a consequence of the huge amount of antigens to which we are exposed every day. The diversity of these immunoglobulins is due to different mechanisms (including VDJ recombination, somatic hypermutation, and antigen selection). Understanding how the immune system is capable of generating this diversity and which are the molecular bases of the composition of immunoglobulins are key challenges in the immunological field. During the last decades, several techniques have emerged as promising strategies to achieve these goals, but it is their combination which appears to be the fruitful solution for increasing the knowledge about human cellular and serum antibody repertoires.In this chapter, we address the diverse strategies focused on the analysis of immunoglobulin repertoires as well as the characterization of the genomic and peptide sequences. Moreover, the advantages of combining various -omics approaches are discussed through review different published studies, showing the benefits in clinical areas.
eng
closedAccess
Proteogenomics
Immunoglobulin sequencing
Antibody repertory
Omics integration
Proteogenomics for the comprehensive analysis of human cellular and serum antibody repertoires
capítulo de libro
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
URL
https://digital.csic.es/bitstream/10261/168690/1/accesoRestringido.pdf
File
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15753
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accesoRestringido.pdf
oai:digital.csic.es:10261/1695862018-09-13T00:54:16Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Brown, Geoffrey
author
Sánchez García, Isidro
2018-09-12T09:08:41Z
2018-09-12T09:08:41Z
2016
Diversity, Versatility, and Leukaemia (2016)
http://hdl.handle.net/10261/169586
The blood cell system has provided a model system that has been used by many researchers to investigate how a stem cell can give rise to a wide variety of mature cell types. The principles that emerged in developmental biology have been applied to the structure of tissues throughout the body. However, many of the principles have been challenged by recent findings, changing the way we view blood cell development. In turn, this has impacted our understanding of the origin and nature of leukaemia, as well as cancer in general. Like the development of any body tissue, cancer is an organised and hierarchical tissue with its own identity. A new viewpoint is that the mutations that give rise to cancer re-programme cancer cells to their own abnormal pattern of tissue development. Understanding how the hierarchy of tumour identity differs from that of normal tissue provides important new avenues to the development of new treatments for cancer. No doubt further refinement to our understanding of normal and cancer cells will continue for many years to come. Even so, we appear to be moving towards an exciting prospect of providing the key to unlocking the long standing mystery of primary cellular events that undermine and distort our normal cells and give rise to the disease of cancer. The importance of this is the prospect of developing new treatments for cancer. In particular, the distorted behaviour of cancer cells might be reversible so that they can be restored to their normal state. Diversity, Versatility and Leukaemia examines how normal and cancer cells are inextricably linked, and focuses on the changes to how we view the development of normal cells and the subversion of this process in cancer.
eng
closedAccess
Diversity, Versatility, and Leukaemia
libro
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URL
https://digital.csic.es/bitstream/10261/169586/1/accesoRestringido.pdf
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oai:digital.csic.es:10261/1695882018-09-13T00:54:57Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Ortega-Carrión, Alvaro
author
Feo-Lucas, L.
author
Vicente-Manzanares, Miguel
2018-09-12T09:13:19Z
2018-09-12T09:13:19Z
2016
Encyclopedia of Cell Biology: 720-730 (2016)
http://hdl.handle.net/10261/169588
Cell migration is a pivotal event during morphogenesis, homeostasis, and disease. Cells can migrate individually or collectively to adapt to their microenvironment and acquire specific migratory modes, for example, mesenchymal, amoeboid, etc. Each migratory mode exhibits different characteristics that endow cells with unique abilities to migrate efficiently through tissues. The ability of a given cell to display a specific migratory mode, or switch among them, is the result of its genetic background and the integration of a wide network of extracellular and intracellular signals that reorganize the plasma membrane and the motile apparatus, i.e., the actin cytoskeleton and the adhesion molecules. Finely tuned migratory events comprise the initial stages of embryo development and organogenesis, and underlie homeostasis, for example, wound healing and the inflammatory response. Pathologic conditions ensue when these carefully orchestrated events are out of tune. Migratory deregulation results in misplaced cells that execute abnormal functions in a foreign microenvironment, for example, leukocyte-mediated tissue damage in autoimmune disease and primary tumor dissemination (metastasis) in cancer. Conversely, strategies aimed at promoting cell migration have the potential to overcome the lack of adaptation of grafted cells to the new microenvironment, for example, during regenerative therapy, that causes migratory defects and overall therapeutic failure.
eng
closedAccess
Cell Migration
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/169588/1/accesoRestringido.pdf
File
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oai:digital.csic.es:10261/1695922020-12-13T09:12:47Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Lazo, Pedro A.
author
Yunta, M.
author
Barcia, R.
2018-09-12T09:22:01Z
2018-09-12T09:22:01Z
2017
Encyclopedia of Signaling Molecules: 566-1-1-566-1-7 (2017)
http://hdl.handle.net/10261/169592
10.1007/978-1-4614-6438-9_566-1
CD53 is one of the least characterized members of the tetraspanin family. CD53 is integrated in the tetraspanin web, and sends intracellular signals, directly or indirectly via PKC, AKT, and g-glutamyl transpeptidase (GGT7). Its expression can affect cell survival, resistance to apoptosis, and radiation sensitivity. In B-cell development CD53 is a marker of mature B cells. In human B-cell malignancies, the pattern of tetraspanin expression identifies the developmental stage of the corresponding tumors. The pattern of tetraspanins can be used to differentiate B-cell malignancies in an individual patient with several lymphoid tumors.
eng
closedAccess
CD53 deficiency
Major histocompatibility complex class
Human leukocyte antigen
CD53 ligation
Homotypic adhesion
CD53
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/169592/1/accesoRestringido.pdf
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application/pdf
accesoRestringido.pdf
oai:digital.csic.es:10261/1695952020-12-13T09:15:46Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Juanes-García, Alba
author
Llorente-González, Clara
author
Vicente-Manzanares, Miguel
funder
Ministerio de Economía y Competitividad (España)
2018-09-12T09:31:01Z
2018-09-12T09:31:01Z
2017
Encyclopedia of Signaling Molecules: 3541-3553 (2017)
http://hdl.handle.net/10261/169595
10.1007/978-1-4614-6438-9_101734-1
http://dx.doi.org/10.13039/501100003329
The discovery of nonmuscle myosin II (NMII) is linked to the story of muscle contraction (reviewed in Szent-Gyorgyi 2004). It started in 1864,...
eng
closedAccess
Myosin head
Actin filament
ATPase activity
Congenital diaphragmatic hernia
Myosin light chain kinase
Nonmuscle myosin II
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/169595/1/accesoRestringido.pdf
File
MD5
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application/pdf
accesoRestringido.pdf
oai:digital.csic.es:10261/1695992020-12-13T09:12:46Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Bustelo, Xosé R.
author
Dosil, Mercedes
2018-09-12T09:47:36Z
2018-09-12T09:47:36Z
2017
Encyclopedia of Signaling Molecules: 1955-2000 (2017)
http://hdl.handle.net/10261/169599
10.1007/978-1-4614-6438-9_513-1
VRK2 is a Ser-Thr kinase and has two isoforms, cytosolic and nuclear. The full-length VRK2 cytosolic isoform (A) inhibits MAPK signaling by a direct interaction with the corresponding JIP1 or KSR1 scaffold proteins. As a consequence, high levels of VRK2A inhibit in a dose-dependent manner signals mediated by the TAK1-MKK7-JNK in response to hypoxia or interleukin, and the signal of the ERBB2-RAS-RAF-MEK-ERK pathway. Downregulation of VRK2A relieves this inhibition and allows signal transmission in response to stimuli initiated in receptor-tyrosine kinases (RTK), such as ERBB2. Thus, in breast cancer VRK2A and ERBB2 present an inverse
correlation.
eng
closedAccess
Skin papilloma
Serum responsive factor
Vulval epithelium
Subfamily GTPases
Intronic single nucleotide polymorphism
Vav family
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/169599/1/accesoRestringido.pdf
File
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accesoRestringido.pdf
oai:digital.csic.es:10261/1696012020-12-13T09:15:25Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Monsalve, Diana M.
author
Blanco, Sandra
author
Fernández, Isabel F.
author
Vázquez-Cedeira, Marta
author
Lazo, Pedro A.
2018-09-12T09:53:36Z
2018-09-12T09:53:36Z
2017
Encyclopedia of Signaling Molecules: 562-2-1-562-2-9 (2017)
http://hdl.handle.net/10261/169601
10.1007/978-1-4614-6438-9_562-2
VRK2 is a Ser-Thr kinase and has two isoforms, cytosolic and nuclear. The full-length VRK2 cyto-solic isoform (A) inhibits MAPK signaling by a direct interaction with the corresponding JIP1 or KSR1 scaffold proteins. As a consequence high levels of VRK2A inhibits in a dose dependent manner signals mediated by the TAK1-MKK7-JNK in response to hypoxia or interleukin, and the signal of the ERBB2-RAS-RAF-MEK-ERK pathway. Downregulation of VRK2A relieves this inhibition and allows signal transmission in response to stimuli initiated in Receptor-tyrosine kinases (RTK), such as ERBB2. Thus, in breast cancer, VRK2A and ERBB2 present an inverse correlation. VRK2 controls protein quality by regulating degradation of misfolded proteins. Mitochondrial VRK2 controls the association of
Bax to mitochondrial membranes and thus modulates apoptosis. Allelic noncoding polymorphisms of the VRK2 gene have been linked to several neurological diseases.
eng
closedAccess
Mitogen activate protein kinase pathway
Vaccinia virus
Mitogen activate protein kinase
Mitogen activate protein kinase signaling
VRK2
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/169601/1/accesoRestringido.pdf
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application/pdf
accesoRestringido.pdf
oai:digital.csic.es:10261/1696022020-12-13T09:12:45Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Cantarero, Lara
author
Moura, David S.
author
Salzano, Marcella
author
Campillo-Marcos, Ignacio
author
Martín-Doncel, Elena
author
Lazo, Pedro A.
2018-09-12T10:00:05Z
2018-09-12T10:00:05Z
2017
Encyclopedia of Signaling Molecules: 561-2-1-561-2-11 (2017)
http://hdl.handle.net/10261/169602
10.1007/978-1-4614-6438-9_561-2
VRK1 is a nuclear chromatin Ser-Thr kinase functionally associated with different processes that require chromatin remodeling. The VRK1 activity is regulated by entry in cell cycle, and this kinase is also required for nuclear envelope dynamics, chromatin condensation, and
Golgi fragmentation. Among its substrates, there are several transcription factors: p53, c-Jun, ATF2, CREB1, and SOX2. VRK1 probably acts cooperating with other signaling pathways that also phosphorylate these transcription factors. VRK1 stabilizes p53 by a specific phosphorylation in Thr18 and after induction of p53 responses, there is a VRK1
downregulation in the lysosome, in which the autophagic pathway participates in a p53-dependent manner. VRK1 also contributes to chromatin condensation, nuclear envelop kinetics by phosphorylation of histone H3 and BAF, and the regulation of Cajal bodies by phosphorylation of coilin. In DNA-damage responses, VRK1 actively participates in chromatin remodeling and regulates H2AX, NBS1, and 53BP1. VRK1 is downstream of MEK1 and Plk3 in the induction of Golgi fragmentation during mitosis. Furthermore, VRK1 is expressed in most tissues, is necessary in the early G1 phase for entry in cell cycle, and is associated with proliferation markers.
eng
closedAccess
Cajal body
Spinal muscular atrophy
Nondividing cell
Amyotrophic lateral sclerosis
VRK1
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/169602/1/accesoRestringido.pdf
File
MD5
42637ae8545636bc41605c1740a9a84e
15753
application/pdf
accesoRestringido.pdf
oai:digital.csic.es:10261/1696042020-12-13T09:15:25Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Moura, David S.
author
Cantarero, Lara
author
Martín-Doncel, Elena
author
Campillo-Marcos, Ignacio
author
Lazo, Pedro A.
2018-09-12T10:09:54Z
2018-09-12T10:09:54Z
2017
Encyclopedia of Signaling Molecules: 563-1-1-563-1-4 (2017)
http://hdl.handle.net/10261/169604
10.1007/978-1-4614-6438-9_563-1
VRK3 is the most divergent member of the VRK family. It has no kinase activity due to several
substitutions in key residues within its catalytic domain. VRK3 is mostly located within the
nucleus and appears to play a scaffold role, where it downregulates MAPK signaling and
reduces the level of p-ERK by recruiting the VHR phosphatase. In addition VRK3 specifically
phosphorylates BAF in Ser4 and induces BAF translocation to cytoplasm. VRK3 expression is
cell cycle regulated, reaching its highest levels in interphase.
eng
closedAccess
Nuclear localization signal
Nuclear envelope
Scaffolding role
Activation loop
Bipartite nuclear localization signal
VRK3
capítulo de libro
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
URL
https://digital.csic.es/bitstream/10261/169604/1/accesoRestringido.pdf
File
MD5
42637ae8545636bc41605c1740a9a84e
15753
application/pdf
accesoRestringido.pdf
oai:digital.csic.es:10261/2211552022-12-23T13:02:58Zcom_10261_2288com_10261_9com_10261_25com_10261_1com_10261_3284com_10261_133com_10261_134com_10261_112com_10261_128com_10261_28457com_10261_3com_10261_41com_10261_47com_10261_8com_10261_79com_10261_64com_10261_80com_10261_33com_10261_5com_10261_70com_10261_2col_10261_2293col_10261_908col_10261_3289col_10261_1016col_10261_1269col_10261_1247col_10261_1263col_10261_28467col_10261_1176col_10261_930col_10261_1214col_10261_947col_10261_1215col_10261_916col_10261_953
DIGITAL.CSIC
author
Montoliu, Lluís
author
Rada-Iglesias, Alvaro
author
Domínguez, María
author
Huertas Sánchez, Pablo
author
Rivas, Javier de las
author
Rojas, A. M.
author
Azorín, Ferran
author
Rotllant, Josep
author
Gutiérrez Armenta, Crisanto
author
Hernández-Munaín, Cristina
author
Barco, Ángel
author
Gómez, María
author
Herrero, Antonia
author
Ramos, Lourdes
author
Fraga, Mario F.
author
Ramos, Sonia
2020-10-14T10:02:33Z
2020-10-14T10:02:33Z
2020
Libro Blanco CSIC 3 (2020)
http://hdl.handle.net/10261/221155
10.20350/digitalCSIC/12650
Our capacity to understand biological systems is restricted by our ability to identify, manipulate and control the genetic information. However, in the last years, great technical advances have extended our capabilities to predict, influence, and to “comprehend” genomic information in virtually every living organism. The ability to identify disease and deleterious genetic and epigenetic traits will reshape biological and biomedical research, and will have implications in how this technical and scientific revolution and the information it will generate may be used in decision-making, about how diseases are diagnosed and treated, and in the decision-making process in reproductive biology
eng
openAccess
Genome and Epigenetics
capítulo de libro
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URL
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oai:digital.csic.es:10261/2211922022-11-15T11:14:18Zcom_10261_2288com_10261_9com_10261_64com_10261_1com_10261_31com_10261_3com_10261_134com_10261_112com_10261_133com_10261_3284com_10261_22com_10261_25com_10261_79com_10261_31891com_10261_2com_10261_92com_10261_7com_10261_93com_10261_4com_10261_120com_10261_81com_10261_5com_10261_89com_10261_132com_10261_8col_10261_2293col_10261_947col_10261_914col_10261_1269col_10261_1247col_10261_1016col_10261_3289col_10261_905col_10261_908col_10261_1214col_10261_31904col_10261_975col_10261_976col_10261_1003col_10261_1216col_10261_1224col_10261_1015
DIGITAL.CSIC
author
Delgado, Mario
author
Ruíz del Árbol, María
author
Durán, Raúl V.
author
Bustelo, Xosé R.
author
Nieto, M. Ángela
author
López, Daniel
author
Gamarro, Francisco
author
Garcillán-Barcia, M. Pilar
author
Varela-Nieto, Isabel
author
Pérez, Belén
author
Molina, Elena
author
Moscoso, Javier
author
Bachiller, Daniel
author
Serrano, María C.
author
Marcos, Susana
author
Herranz, Fernando
author
D’Este, Pablo
2020-10-14T13:51:13Z
2020-10-14T13:51:13Z
2020
Libro Blanco CSIC 4 (2020)
http://hdl.handle.net/10261/221192
10.20350/digitalCSIC/12651
Something that we have learned from the pandemia caused by coronavirus isthat solutionsin healthrequire coordinated actions. Beside this and other (re)emerging infectious diseases, spain and europe are suffereng a plethora of disorders that are actually adquiring epidemic dimensions, including cancer, rare disesases, pain and food allergies between others. New tools for prevention, diagnosis and treatment need to be urgently designed and implemented using new holistic and multidisciplinary approaches that involve researchers, clinicials, industryand all stakeholthersof health system. CSIC is excellently positioned to lead and coordinate these challengesin Biomedicine and Health.
spa eng
openAccess
Challenges in Biomedicine and Health
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/221192/3/VOLUMEN%204.pdf
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VOLUMEN 4.pdf
oai:digital.csic.es:10261/2340592022-11-20T05:30:30Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Talayero, Vanessa C.
author
Vicente-Manzanares, Miguel
funder
Ministerio de Ciencia, Innovación y Universidades (España)
funder
Agencia Estatal de Investigación (España)
funder
Asociación Española Contra el Cáncer
funder
Junta de Castilla y León
2021-03-10T16:10:15Z
2021-03-10T16:10:15Z
2020
Methods in molecular biology (Clifton, N.J.) 2217: 27-37 (2020)
1940-6029
http://hdl.handle.net/10261/234059
10.1007/978-1-0716-0962-0_3
http://dx.doi.org/10.13039/501100011033http://dx.doi.org/10.13039/501100014180
Focal adhesions in planar substrates constitute an excellent cellular resource to evaluate different parameters related to cell morphology, cytoskeletal organization, and adhesive strength. However, their intrinsic heterogeneity in terms of size, molecular composition, orientation, and so on complicates their analysis. Here, we describe a simple and straightforward ImageJ/Fiji-based method to quantify several parameters that describe the morphology and relative composition of focal adhesions. This type of analysis can be implemented in various ways and become useful for drug and shRNA screenings.
openAccess
Focal adhesion
Protrusion
Actin cytoskeleton
ImageJ
Multiparametric Analysis of Focal Adhesions in Bidimensional Substrates
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/234059/4/Multi-parametric_Talayero_CapLib2020.pdf
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application/pdf
Multi-parametric_Talayero_CapLib2020.pdf
oai:digital.csic.es:10261/2497872022-10-24T14:13:47Zcom_10261_112com_10261_1com_10261_25com_10261_128com_10261_131com_10261_2col_10261_1247col_10261_908col_10261_1263col_10261_1266
DIGITAL.CSIC
author
Rivas, Javier de las
author
Rojas, A. M.
author
Montoliu, Lluís
author
Mora, Leticia
author
Pazos, Florencio
2021-09-09T06:45:03Z
2021-09-09T06:45:03Z
2021
Genome & Epigenetics 3(2): 28-49 (2021)
978-84-00-10739-0
http://hdl.handle.net/10261/249787
High-throughput omics technologies are called to revolutionize medical practice by the general implementation of precision and personalized medicine (PPM) approaches to tailor diagnostic, therapeutic and monitoring
strategies for individual patients based on their genetic and molecular signatures.
spa
openAccess
Omics
Big data
Precision medicine
Personalized medicine
Omics technologies and precision medicine
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/249787/1/omicsmedicine.pdf
File
MD5
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application/pdf
omicsmedicine.pdf
oai:digital.csic.es:10261/2505982022-12-20T13:30:44Zcom_10261_64com_10261_1com_10261_134com_10261_105com_10261_54com_10261_86com_10261_112com_10261_22col_10261_947col_10261_1269col_10261_1240col_10261_937col_10261_1221col_10261_1247col_10261_905
DIGITAL.CSIC
author
Álvarez-Dolado, Manuel
author
Casas-Tinto, Sergio
author
Corbí, Angel L.
author
De Las Rivas, Javier
author
Delgado, Manuel
author
Fuentes-García, Manuel
author
González-Rey, Elena
author
Iglesias, Teresa
author
Llebaria, Amadeu
author
López-Atalaya, José P.
author
Mittelbrunn, M.
author
Rocón, Eduardo
author
Serrano, Teresa
author
Villa, Rosa
author
Yúfera, Alberto
author
Duarte, Esther
author
Gil-Agudo, Ángel
author
Planas, Anna M.
author
Moreno, Juan Camilo
2021-09-20T11:30:03Z
2021-09-20T11:30:03Z
2021
White Paper 5: Brain, Mind and Behaviour: 107- 123 (2021)
http://hdl.handle.net/10261/250598
Stroke and traumatic injury in brain or spinal
cord are often life-threating conditions and
major causes of death or permanent disability
with high impact in the health care system.
There are several stages of intervention to
improve the neurological outcome. Acutely, fast
interventions aiming to reestablish cerebral
blood flow in ischemic stroke, to stop bleeding
after brain hemorrhage, and to reduce edema
after contusions are amongst mandatory
actions. Current studies aim to develop
accompanying strategies for brain cell
protection based on enhancing endogenous
protective mechanism, blocking cell death
pathways, or through immunomodulation.
After the acute phase, interventions are
intended to promote recovery of function using
rehabilitation with state-of-the-art
technologies enabled by robotics. Other
advanced strategies include cell, gene, and
immune therapies, and brain function
modulation with the aid of smart
nanotechnologies. There is great expectation in
the fast evolving novel approaches for
improvement of neurological deficits in these
unpredictable and devastating condition
closedAccess
troke traumatic brain injurybiomarkers for CNS injury neuroplasticityneural repair neural regenerationneurorehabilitation technologyneuroinflammation neuroprotection
BRAIN & SPINAL CORD DAMAGE & REHABILITATION
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/250598/1/accesoRestringido.pdf
File
MD5
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15753
application/pdf
accesoRestringido.pdf
oai:digital.csic.es:10261/2514202021-10-04T06:35:21Zcom_10261_133com_10261_1com_10261_134com_10261_112com_10261_109com_10261_3284com_10261_25col_10261_1016col_10261_1269col_10261_1247col_10261_1244col_10261_3289col_10261_908
DIGITAL.CSIC
author
Domínguez, María
author
Huertas Sánchez, Pablo
author
Casado, Marta
author
López-Atalaya, José P.
author
Pendás, Alberto M.
author
Montoliu, Lluís
author
Ros, Marian
2021-10-01T11:23:09Z
2021-10-01T11:23:09Z
2021
Genome & Epigenetics 3(1): 10-27 (2021)
978-84-00-10738-3
http://hdl.handle.net/10261/251420
During the last few decades, the genomes from hundreds of different living organisms have been fully sequenced. Decoding this vast amount of genetic information promises to unlock the molecular secrets of life in our planet as well as the molecular basis of human disease. However, this is far from trivial since in many species the protein-coding sequences (i.e. genes) only account for a small fraction of their genome, with the remaining non-coding sequences potentially playing regulatory functions. Moreover, within multicellular organisms, the genome is uniquely used in each cell type by
introducing epigenetic modifications and/or adopting particular 3D conformations that can affect gene activity and expression without changing the underlying DNA sequences. Despite this complexity, recent advances in various -omics and genome editing technologies have dramatically improved our current understanding of genome function.
Therefore, we are now in a unique position to sequence, analyze and modify genomes, and, thus, to improve not only our quality of life but also that of our planet.
eng
openAccess
Methods to analyse and modify the genome
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/251420/1/methodsgenome.pdf
File
MD5
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application/pdf
methodsgenome.pdf
oai:digital.csic.es:10261/2514452022-03-14T09:33:16Zcom_10261_133com_10261_1com_10261_79com_10261_112com_10261_109com_10261_41com_10261_22col_10261_1016col_10261_1214col_10261_1247col_10261_1244col_10261_1176col_10261_905
DIGITAL.CSIC
author
Barco, Ángel
author
Gómez Vicentefranqueira, María
author
Blanco, Sandra
author
Gómez-Díaz, Elena
author
Martín, J.
author
Martínez Balbás, Marián
author
Pérez-Tur, Jordi
author
Sánchez García, Isidro
author
Suñé, Carlos
author
Vallejo, Mario
2021-10-04T06:47:10Z
2021-10-04T06:47:10Z
2021
Genome & Epigenetics 3(5): 102-121 (2021)
978-84-00-10738-3
http://hdl.handle.net/10261/251445
In recent years, there have been great efforts to characterize the epigenome and
epitranscriptome of different cell types and organisms. However, most of those studies are descriptive and we still ignore the role of many epi-modifications. We discuss the need of gaining functional and mechanistic insight and the large impact that this knowledge will have in the understanding and treatment of numerous diseases.
eng
openAccess
Functional epigenetics and epitranscriptomics and their role in health and disease
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/251445/1/funtionadisea.pdf
File
MD5
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189714
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funtionadisea.pdf
oai:digital.csic.es:10261/2598262022-11-15T11:25:05Zcom_10261_134com_10261_1com_10261_120com_10261_7com_10261_112com_10261_3284com_10261_31891com_10261_2com_10261_31com_10261_3com_10261_132com_10261_8com_10261_2288com_10261_9col_10261_1269col_10261_1003col_10261_1247col_10261_3289col_10261_31904col_10261_914col_10261_1015col_10261_2293
DIGITAL.CSIC
author
Marco de Lucas, Jesús Eugenio
author
Moreno-Arribas, M. Victoria
author
Delgado, Mario
author
Ruíz del Árbol, María
author
Durán, Raúl V.
author
Bustelo, Xosé R.
author
Nieto, M. Ángela
author
López, Daniel
author
Gamarro, Francisco
author
Garcillán-Barcia, M. Pilar
author
Varela-Nieto, Isabel
author
Pérez, Belén
author
Molina, Elena
author
Moscoso, Javier
author
Bachiller, Daniel
author
Serrano, María C.
author
Marcos, Susana
author
Castro, Alberto de
author
Herranz, Fernando
author
D’Este, Pablo
2022-02-03T17:40:04Z
2022-02-03T17:40:04Z
2021
White Paper 4: Challenges in Biomedicine and Health (2021)
http://hdl.handle.net/10261/259826
A lesson that we have learned from the pandemia caused by coronavirus is that solutions in health require coordinated actions. Beside this and other emerging and re-emerging infectious diseases, millions of Europeans are suffering a plethora of disorders that are currently acquiring epidemic dimensions, including cancer, rare diseases, pain and food allergies, among others. New tools for prevention, diagnosis and treatment need to be urgently designed and implemented using new holistic and multidisciplinary approaches at three different levels (basic research, translational/clinical and public/social levels) and involving researchers, clinicians, industry and all stakeholders in the health system. The CSIC is excellently positioned to lead and coordinate these challenges in Biomedicine and Health.
openAccess
White Paper 4: Challenges in Biomedicine and Health
libro
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URL
https://digital.csic.es/bitstream/10261/259826/3/biomedicine_health.pdf
File
MD5
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application/pdf
biomedicine_health.pdf
oai:digital.csic.es:10261/2599862022-11-04T17:07:22Zcom_10261_41com_10261_1com_10261_133com_10261_33com_10261_5com_10261_25com_10261_128com_10261_134com_10261_28457com_10261_3com_10261_80com_10261_70com_10261_2com_10261_47com_10261_8com_10261_112com_10261_64com_10261_3284com_10261_109com_10261_2288com_10261_9col_10261_1176col_10261_1016col_10261_916col_10261_908col_10261_1263col_10261_1269col_10261_28467col_10261_1215col_10261_953col_10261_930col_10261_1247col_10261_947col_10261_3289col_10261_1244col_10261_2293
DIGITAL.CSIC
author
Marco de Lucas, Jesús Eugenio
author
Moreno-Arribas, M. Victoria
author
Montoliu, Lluís
author
Rada-Iglesias, Alvaro
author
Domínguez, María
author
Huertas Sánchez, Pablo
author
Rivas, Javier de las
author
Rojas, A. M.
author
Azorín, Ferran
author
Rotllant, Josep
author
Gutiérrez Armenta, Crisanto
author
Hernández-Munaín, Cristina
author
Barco, Ángel
author
Gómez, María
author
Herrero, Antonia
author
Ramos, Lourdes
author
Fraga, Mario F.
author
Ramos, Sonia
2022-02-07T09:00:03Z
2022-02-07T09:00:03Z
2021
White Paper 3: Genome and Epigenetics (2021)
978-84-00-10739-0
978-84-00-10738-3978-84-00-10738-3
http://hdl.handle.net/10261/259986
During the last few decades, the genomes from hundreds of different living organisms have been fully sequenced. Decoding this vast amount of genetic information promises to unlock the molecular secrets of life in our planet as well as the molecular basis of human disease. However, this is far from trivial since in many species the protein-coding sequences (i.e. genes) only account for a small fraction of their genome, with the remaining non-coding sequences potentially playing regulatory functions. Moreover, within multicellular organisms, the genome is uniquely used in each cell type by introducing epigenetic modifications and/or adopting particular 3D conformations that can affect gene activity and expression without changing the underlying DNA sequences. Despite this complexity, recent advances in various -omics and genome editing technologies have dramatically improved our current understanding of genome function. Therefore, we are now in a unique position to sequence, analyze and modify genomes, and, thus, to improve not only our quality of life but also that of our planet.
openAccess
Genomics
Epigenetics
Epigenomics
Epitranscriptomics
Genome archictecture
Genome editing
Non-coding genome
Precision medicine
Metagenomics
Microbiota
Life style
Environmental genomics
White Paper 3: Genome and Epigenetics
libro
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URL
https://digital.csic.es/bitstream/10261/259986/4/Genome_epigenetics.pdf
File
MD5
e25db50890cb6b563b0b59c7f332f976
1692031
application/pdf
Genome_epigenetics.pdf
oai:digital.csic.es:10261/2609492022-02-17T02:47:07Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Usategui-Martín, Ricardo
author
Rodríguez-Hernández, Irene
author
González-Sarmiento, Rogelio
author
Sobas, Eva M.
author
Pastor, Jose Carlos
author
Pastor-Idoate, Salvador
2022-02-16T08:40:03Z
2022-02-16T08:40:03Z
2021
Methods in molecular biology 2248: 243-250 (2021)
978-1-0716-1129-6
978-1-0716-1130-2
http://hdl.handle.net/10261/260949
10.1007/978-1-0716-1130-2_18
With the evolution of new genomic sequencing technologies an important amount of genomic data has been provided. As a consequence of this, many gene polymorphisms have been shown to be significantly associated with different disorders. Many strategies have been implemented to reveal the role of having more than one allele at a specific locus and their involvement in the illnesses. Site-directed mutagenesis is one of the most common strategies to understand the regulatory regions of genes and the relationship between the protein structure and its function. Here, we describe the analysis of lymphotoxin alpha expression in human retina and the generation of expression vectors to functional characterization of polymorphisms in the tumor necrosis factor locus using pCEFL-Flag expression vector and transfection assays in COS-1 cell line.
closedAccess
Tumor necrosis factor
Lymphotoxin alpha
LTA
Retina
Functional characterization
Polymorphisms
Site-directed mutagenesis
Expression vectors and pCEFL-Flag
Analysis of Lymphotoxin Alpha Expression in Human Retina and Generation of Expression Vectors to Functional Characterization of Polymorphisms in the Tumor Necrosis Factor Locus
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/260949/1/accesoRestringido.pdf
File
MD5
42637ae8545636bc41605c1740a9a84e
15753
application/pdf
accesoRestringido.pdf
oai:digital.csic.es:10261/2616832022-02-24T02:46:54Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Cobaleda, César
author
Sánchez García, Isidro
funder
European Commission
funder
Ministerio de Economía y Competitividad (España)
funder
Fundación Ramón Areces
funder
Fundación Síndrome de Wolf-Hirschhorn
funder
Banco Santander
funder
Agencia Estatal de Investigación (España)
funder
Ministerio de Ciencia, Innovación y Universidades (España)
funder
Junta de Castilla y León
funder
Josep Carreras Leukemia Foundation
funder
Fundación Unoentrecienmil
2022-02-23T10:10:24Z
2022-02-23T10:10:24Z
2021
Methods in molecular biology 2185: 39-48 (2021)
978-1-0716-0809-8
http://hdl.handle.net/10261/261683
10.1007/978-1-0716-0810-4_3
1940-6029
http://dx.doi.org/10.13039/501100003329http://dx.doi.org/10.13039/501100011033http://dx.doi.org/10.13039/100010784http://dx.doi.org/10.13039/501100000780http://dx.doi.org/10.13039/100008054http://dx.doi.org/10.13039/501100005677http://dx.doi.org/10.13039/501100014180
The relative survival of cancer patients, when considering the tumoral stage at diagnosis, has not changed significantly in the last three decades, in spite of our increasingly detailed knowledge of the molecular alterations occurring in human tumors. In parallel, despite a growing number of clinical trials being conducted, the absolute number of drugs that are effective in humans is declining, and many new drugs move into the market without having enough evidence of their benefit on survival or quality of life. In part, this failure is due to the discordance between the results from preclinical and clinical trial phases, therefore leading to a high percentage of apparently promising lead compounds being abandoned in the transfer to the clinic. This discordance is caused, to a large degree, by the use of inappropriate animal models in the first stages of drug development. In this chapter, we discuss how the development of cancer therapies needs to be redesigned in order to achieve cancer cure, and how this redesign must involve the generation of better animal models, based on the tenets of the cancer stem cell theory, and capable of recapitulating all the aspects of human cancer. The use of such improved models should increase the likelihood of success in drug development, reducing the number of agents that go into trial, and the amount of patients undergoing useless trials.
closedAccess
Leukemic stem cells
Cancer stem cells
Epigenetic reprogramming
Leukemia
Animal models
Leukemia Stem Cell Drug Discovery
artículo
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URL
https://digital.csic.es/bitstream/10261/261683/1/accesoRestringido.pdf
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accesoRestringido.pdf
oai:digital.csic.es:10261/2616982022-02-24T02:47:15Zcom_10261_112com_10261_1com_10261_79col_10261_1247col_10261_1214
DIGITAL.CSIC
author
Sánchez García, Isidro
author
Cobaleda, César
funder
European Commission
funder
Ministerio de Ciencia, Innovación y Universidades (España)
funder
Fundación Ramón Areces
funder
Fundación Síndrome de Wolf-Hirschhorn
funder
Banco Santander
funder
Junta de Castilla y León
funder
Josep Carreras Leukemia Foundation
funder
Federal Office for Radiation Protection (Germany)
funder
Fundación Unoentrecienmil
2022-02-23T10:40:16Z
2022-02-23T10:40:16Z
2021
Methods in molecular biology 2185: 25-37 (2021)
978-1-0716-0809-8
http://hdl.handle.net/10261/261698
10.1007/978-1-0716-0810-4_2
http://dx.doi.org/10.13039/501100006529http://dx.doi.org/10.13039/100010784http://dx.doi.org/10.13039/501100000780http://dx.doi.org/10.13039/501100014180http://dx.doi.org/10.13039/100008054http://dx.doi.org/10.13039/501100005677
Only 10 years ago, the existence of cancer stem cells (CSCs) was still hotly debated. Even today, when their presence in most tumor types has been clearly demonstrated, all the consequences of their existence are far from being realized neither in the clinic nor, very often, in basic and translational cancer research. The existence of CSCs supposes a true change of paradigm in our understanding of cancer, but it will only have a real impact when we will properly assimilate its implications and apply these insights to both cancer research and cancer treatment. In this primer to the topic of leukemia stem cells (LSCs) our aim is to highlight with broad brushstrokes the most relevant of their properties, how these characteristics led to their identification, and the implications that the existence of LSCs has for the research and fight against leukemia.
closedAccess
Leukemic stem cells
Cancer stem cells
Epigenetic reprogramming
Leukemia
Animal models
Leukemia Stem Cells: Concept and Implications
artículo
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URL
https://digital.csic.es/bitstream/10261/261698/1/accesoRestringido.pdf
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accesoRestringido.pdf
oai:digital.csic.es:10261/2640122022-10-13T08:50:45Zcom_10261_112com_10261_1col_10261_1247
DIGITAL.CSIC
author
Vicente-Manzanares, Miguel
2022-03-15T08:36:44Z
2022-03-15T08:36:44Z
2021
The integrin interactome (2021)
978-1-0716-0961-3
1064-3745
http://hdl.handle.net/10261/264012
10.1007/978-1-0716-0962-0
closedAccess
The integrin interactome
libro
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15753
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accesoRestringido.pdf
oai:digital.csic.es:10261/3070102023-04-21T07:05:22Zcom_10261_112com_10261_1com_10261_79com_10261_25col_10261_1247col_10261_1214col_10261_908
DIGITAL.CSIC
author
Antón, Inés María
author
Wandosell, Francisco
author
Vicente-Manzanares, Miguel
funder
Fundación Ramón Areces
funder
Ministerio de Ciencia, Innovación y Universidades (España)
funder
Agencia Estatal de Investigación (España)
funder
European Commission
funder
Asociación Española Contra el Cáncer
funder
Junta de Castilla y León
2023-04-21T07:00:18Z
2023-04-21T07:00:18Z
2022
Cell movement in Health and Disease: 245-270 (2022)
http://hdl.handle.net/10261/307010
Acquisition of motile capability is one of the most tantalizing features of the oncogenic cell transformation program. Cancer cell migration borrows heavily from normal morphogenetic processes that are activated during embryonic differentiation and tissue growth. Tumor cell migration is triggered by genetic modifications that activate transcriptional programs, e.g., the epithelial–mesenchymal transition, which lie dormant in healthy tissues. These programs allow cells to generate structures that enable them to move and manipulate the extracellular matrix to favor their dissemination, e.g., invadopodia. Collectively, these processes not only affect the cancer cells themselves, but also trigger modifications of the tumor microenvironment, aggressively promoting tumor growth and dissemination. As such, cancer cell migration not only depends on the genetic changes that are the most important element of oncogenic transformation; but it is also influenced by the mechanochemical makeup of the tumor microenvironment. In this chapter, we describe the changes that enable tumor cells to become migratory. We also address the cellular and acellular composition of the tumor microenvironment as it controls cancer growth and migration, from small tumors made of a few cells to large, invasive masses that have the ability to form distal metastasis.
closedAccess
Extracellular matrix
Invadopodia
Mechanotransduction
Migratory signaling
Tumor microenvironment
Tumor-associated cells
Chapter 15 - Cancer cell development, migratory response, and the role of the tumor microenvironment in invasion and metastasis
capítulo de libro
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URL
https://digital.csic.es/bitstream/10261/307010/1/accesoRestringido.pdf
File
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42637ae8545636bc41605c1740a9a84e
15753
application/pdf
accesoRestringido.pdf