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dc.contributor.author | Fonteriz, Rosalba I. | - |
dc.contributor.author | Matesanz-Isabel, Jessica | - |
dc.contributor.author | Arias-del-Val, Jessica | - |
dc.contributor.author | Alvarez-Illera, Pilar | - |
dc.contributor.author | Montero, Mayte | - |
dc.contributor.author | Álvarez, Javier | - |
dc.date.accessioned | 2017-12-11T13:41:32Z | - |
dc.date.available | 2017-12-11T13:41:32Z | - |
dc.date.issued | 2016 | - |
dc.identifier | doi: 10.1007/978-3-319-26974-0_17 | - |
dc.identifier | isbn: 978-3-319-26972-6 | - |
dc.identifier.citation | Calcium Entry Pathways in Non-excitable Cells: 405-421 (2016) | - |
dc.identifier.uri | http://hdl.handle.net/10261/158077 | - |
dc.description.abstract | The role of mitochondria in intracellular Ca(2+) signaling relies mainly in its capacity to take up Ca(2+) from the cytosol and thus modulate the cytosolic [Ca(2+)]. Because of the low Ca(2+)-affinity of the mitochondrial Ca(2+)-uptake system, this organelle appears specially adapted to take up Ca(2+) from local high-Ca(2+) microdomains and not from the bulk cytosol. Mitochondria would then act as local Ca(2+) buffers in cellular regions where high-Ca(2+) microdomains form, that is, mainly close to the cytosolic mouth of Ca(2+) channels, both in the plasma membrane and in the endoplasmic reticulum (ER). One of the first targets proposed already in the 1990s to be regulated in this way by mitochondria were the store-operated Ca(2+) channels (SOCE). Mitochondria, by taking up Ca(2+) from the region around the cytosolic mouth of the SOCE channels, would prevent its slow Ca(2+)-dependent inactivation, thus keeping them active for longer. Since then, evidence for this mechanism has accumulated mainly in immunitary cells, where mitochondria actually move towards the immune synapse during T cell activation. However, in many other cell types the available data indicate that the close apposition between plasma and ER membranes occurring during SOCE activation precludes mitochondria from getting close to the Ca(2+)-entry sites. Alternative pathways for mitochondrial modulation of SOCE, both Ca(2+)-dependent and Ca(2+)-independent, have also been proposed, but further work will be required to elucidate the actual mechanisms at work. Hopefully, the recent knowledge of the molecular nature of the mitochondrial Ca(2+) uniporter will allow soon more precise studies on this matter. | - |
dc.description.sponsorship | This work was supported by a grant from the Spanish Ministerio de Ciencia e Innovación (BFU2011-25763). Jessica Matesanz-Isabel holds a FPI (Formación de Personal Investigador) fellowship from the Spanish Government. Jessica Arias-del-Val holds a fellowship from Junta de Castilla y León. | - |
dc.publisher | Springer Nature | - |
dc.relation.ispartofseries | Advances in Experimental Medicine and Biology 898 | - |
dc.relation.isversionof | Preprint | - |
dc.rights | openAccess | - |
dc.subject | Mitochondria | - |
dc.subject | Store-operated Ca2+ entry | - |
dc.subject | SOCE | - |
dc.subject | Endoplasmic reticulum | - |
dc.subject | STIM | - |
dc.subject | MCU | - |
dc.subject | Ca2+ uniporter Ca2+ microdomain | - |
dc.subject | CRAC channels | - |
dc.subject | Orai | - |
dc.title | Modulation of calcium entry by mitochondria | - |
dc.type | capítulo de libro | - |
dc.identifier.doi | 10.1007/978-3-319-26974-0_17 | - |
dc.relation.publisherversion | https://doi.org/10.1007/978-3-319-26974-0_17 | - |
dc.date.updated | 2017-12-11T13:41:32Z | - |
dc.description.version | Peer Reviewed | - |
dc.language.rfc3066 | eng | - |
dc.contributor.funder | Ministerio de Ciencia e Innovación (España) | - |
dc.contributor.funder | Junta de Castilla y León | - |
dc.relation.csic | Sí | - |
dc.identifier.funder | http://dx.doi.org/10.13039/501100004837 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/501100014180 | es_ES |
dc.type.coar | http://purl.org/coar/resource_type/c_3248 | es_ES |
item.fulltext | With Fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.cerifentitytype | Publications | - |
item.grantfulltext | open | - |
item.openairetype | capítulo de libro | - |
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