2005
DOI: 10.1074/jbc.m411507200
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Extracellular pH Modifies Mitochondrial Control of Capacitative Calcium Entry in Jurkat Cells

Abstract: It was found that a collapse of the mitochondrial calcium buffering caused by the protonophoric uncoupler CCCP, antimycin A plus oligomycin, or the inhibitor of the mitochondrial Ca 2؉ /Na ؉ exchanger led to a strong inhibition of thapsigargin-induced capacitative Ca

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Cited by 15 publications
(11 citation statements)
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“…I CRAC in human monocyte-derived macrophages shows an extracellular pH-dependent change of current amplitude with a pK a of 8.2 [40]. Two studies in Jurkat T lymphocytes suggest that extracellular pH modifies the mitochondrial control of SOCE in Jurkat cells [41,42]. Others predict a similar mechanism as assumed for L-type Ca 2+ channels via the protonation of negatively charged glutamate residues close to the channel pore [43,44].…”
Section: Introductionmentioning
confidence: 99%
“…I CRAC in human monocyte-derived macrophages shows an extracellular pH-dependent change of current amplitude with a pK a of 8.2 [40]. Two studies in Jurkat T lymphocytes suggest that extracellular pH modifies the mitochondrial control of SOCE in Jurkat cells [41,42]. Others predict a similar mechanism as assumed for L-type Ca 2+ channels via the protonation of negatively charged glutamate residues close to the channel pore [43,44].…”
Section: Introductionmentioning
confidence: 99%
“…The released Ca 2+ from ER or sarcoplasmic reticulum (SR) enters mitochondria and the subsequent rise of mitochondrial Ca 2+ activates several mitochondrial dehydrogenases (Jo et al 2006; Csordas & Hajnoczky, 2009). The mitochondrial Ca 2+ sequestration and/or the mitochondrial metabolites have been reported to fine‐tune the amplitude of SOCE (Hoth et al 1997; Zablocki et al 2005; Parekh, 2008; Schwindling et al 2010). Interestingly, mitochondria accumulate in the vicinity of immunological synapses in Jurkat T cells upon T cell receptor activation (Quintana et al 2007).…”
Section: Introductionmentioning
confidence: 99%
“…To fulfill these functions, mitochondria must generate a high electrochemical proton gradient (⌬⌿) across the inner membrane. Their de-energization due to inhibition of the respiratory chain or to uncoupling of oxidative phosphorylation may result in cellular energy deficiency and impairment of ⌬⌿-dependent processes, among them intracellular calcium signaling (11,15,26,27). In metazoa mitochondrial DNA (mtDNA) typically encodes 13 proteins involved in oxidative phosphorylation; two of them are elements of the F o subunit of mitochondrial ATPase, while 11 proteins are components of the respiratory chain complexes I, III, and IV.…”
mentioning
confidence: 99%