<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-04-23T20:28:53Z</responseDate><request verb="GetRecord" identifier="oai:uvadoc.uva.es:10324/6348" metadataPrefix="etdms">http://uvadoc.uva.es/oai/request</request><GetRecord><record><header><identifier>oai:uvadoc.uva.es:10324/6348</identifier><datestamp>2021-06-23T09:51:57Z</datestamp><setSpec>com_10324_1134</setSpec><setSpec>com_10324_931</setSpec><setSpec>com_10324_894</setSpec><setSpec>col_10324_1213</setSpec></header><metadata><thesis xmlns="http://www.ndltd.org/standards/metadata/etdms/1.0/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.ndltd.org/standards/metadata/etdms/1.0/ http://www.ndltd.org/standards/metadata/etdms/1.0/etdms.xsd">
<title>The coupling of plasma membrane calcium entry to calcium uptake by endoplasmic reticulum and mitochondria</title>
<creator>García-Sancho Martín, Francisco Javier</creator>
<subject>Calcio - Absorción</subject>
<description>Producción Científica</description>
<description>Cross-talk between organelles and plasma membrane Ca2+ channels is essential for&#xd;
modulation of the cytosolic Ca2+ ([Ca2+]C) signals, but such modulation may differ among&#xd;
cells. In chromaffin cells Ca2+ entry through voltage-operated channels induces calcium release&#xd;
from the endoplasmic reticulum (ER) that amplifies the signal. [Ca2+]C microdomains as high&#xd;
as 20–50 μM are sensed by subplasmalemmal mitochondria, which accumulate large amounts of&#xd;
Ca2+ through the mitochondrial Ca2+ uniporter (MCU). Mitochondria confine the high-Ca2+&#xd;
microdomains (HCMDs) to beneath the plasma membrane,where exocytosis of secretory vesicles&#xd;
happens. Cell core [Ca2+]C is much smaller (1–2 μM). By acting as a Ca2+ sink, mitochondria&#xd;
stabilise theHCMDin space and time. In non-excitableHEK293 cells, activation of store-operated&#xd;
Ca2+ entry, triggered by ERCa2+ emptying, also generated subplasmalemmal HCMDs, but, in this&#xd;
case, most of the Ca2+ was taken up by the ER rather than bymitochondria. The smaller size of the&#xd;
[Ca2+]C peak in this case (about 2 μM)may contribute to this outcome, as the sarco-endoplasmic&#xd;
reticulum Ca2+ ATPase has much higher Ca2+ affinity than MCU. It is also possible that the relative positioning of organelles, channels and effectors, as well as cytoskeleton and accessory&#xd;
proteins plays an important role.</description>
<date>2014-09-30</date>
<date>2015-09-30</date>
<date>2014</date>
<type>info:eu-repo/semantics/article</type>
<identifier>Journal of Physiology, 2014, p. 261-268</identifier>
<identifier>0022-3751</identifier>
<identifier>http://uvadoc.uva.es/handle/10324/6348</identifier>
<identifier>10.1113/jphysiol.2013.255661</identifier>
<identifier>261</identifier>
<identifier>268</identifier>
<identifier>Journal of Physiology</identifier>
<language>eng</language>
<rights>info:eu-repo/semantics/openAccess</rights>
<rights>http://creativecommons.org/licenses/by-nc-nd/4.0/</rights>
<rights>Attribution-NonCommercial-NoDerivatives 4.0 International</rights>
<publisher>The Physiological Society</publisher>
</thesis></metadata></record></GetRecord></OAI-PMH>