2024-03-28T10:00:54Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1238312016-02-18T03:35:57Zcom_10261_134com_10261_1col_10261_513
Uncovering the network that controls double strand break repair pathway choice
Huertas Sánchez, Pablo
Gómez-Cabello, Daniel
Jimeno, Sonia
Fernández-Ávila, María Jesús
Póster presentado al 22nd IUBMB & 37th FEBS Congress: From Single Molecules to Systems Biology, celebrado en Sevilla (España) del 4 al 9 de septiembre de 2012
Double strand breaks (DSBs) repair is essential for normal development.
While the complete inability to repair DSBs leads to
embryonic lethality and cell death, mutations that hamper this
repair cause genetically inherited syndromes, with or without cancer
predisposition. The phenotypes associated with these syndromes
are extremely varied, and can include growth and mental
retardation, ataxia, skeletal abnormalities, immunodeficiency,
premature aging, etc.
DSBs are repaired by two major mechanisms that compete for
the same substrate. Both ends of the DSB can be simple re-joined with little or no processing, a mechanism known as non-homologous
end-joining. On the other hand, DSBs can be processed and
engaged in a more complex repair pathway called homologous
recombination. This pathway uses the information present in a
homologue sequence. The balance between these two pathways is
exquisitely controlled and its alteration leads to the appearance
of chromosomal abnormalities and contribute to the diseases
aforementioned. However, and despite its importance, the network
controlling the choice between both is poorly understood.
Here, we present a novel system specifically designed to unravel
how the choice between both DSBs repair pathways is made,
and its relevance for cellular and organismal survival, disease and
development.
Peer Reviewed
2015-10-26T11:50:18Z
2015-10-26T11:50:18Z
2012-09-04
2015-10-26T11:50:19Z
póster de congreso
http://purl.org/coar/resource_type/c_6670
22nd IUBMB - 37th FEBS Congress (2012)
http://hdl.handle.net/10261/123831
Sí
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