Store-Operated Ca2+ Entry

Berna‐Erro, Alejandro; Redondo, Pedro C.; Rosado, Juan A.

doi:10.1007/978-94-007-2888-2_15

Cited by 48 publications

(30 citation statements)

References 263 publications

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“…Orai1 is a tetrameric selective Ca 2+ channel in the plasma membrane and mediates the voltage-independent Ca 2+ influx referred to as the Ca 2+ -activated Ca 2+ current (CRAC) and responsible for the previously called capacitative Ca 2+ entry [187][188][189]. The roles of STIM2, Orai2 and Orai3 in the control of SOC are less well clarified [185,187]. Some TRPC channels (canonical transient receptor potential) also produce a SOC.…”

Section: Impact Of [Ca 2+ ] Er On Ca 2+ Influx: Store-operated Ca 2+ mentioning

confidence: 98%

“…One type of current is mediated by the interaction of STIM (stromal interaction molecule) and Orai proteins for which several isoforms have been described (2 for STIM and 3 for Orai) (Fig. 1) [185]. STIM are ubiquitously expressed single-pass transmembrane ER proteins with a luminal Ca 2+ sensor [186].…”

Section: Impact Of [Ca 2+ ] Er On Ca 2+ Influx: Store-operated Ca 2+ mentioning

confidence: 99%

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Calcium signaling in pancreatic β-cells in health and in Type 2 diabetes

et al. 2014

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Section: Impact Of [Ca 2+ ] Er On Ca 2+ Influx: Store-operated Ca 2+ mentioning

confidence: 98%

Section: Impact Of [Ca 2+ ] Er On Ca 2+ Influx: Store-operated Ca 2+ mentioning

confidence: 99%

Calcium signaling in pancreatic β-cells in health and in Type 2 diabetes

et al. 2014

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“…Although predominantly thought of in the context of non-excitable cells, store-operated Ca 2ϩ entry (SOCE) by store-operated channels (SOCs) has recently emerged as a potential mechanism to alter Ca 2ϩ in the diseased cardiomyocyte. Although still under debate, the prime candidate proteins for SOCs encompass the TRPC channel(s) as non-selective cation channels as well as Orai1, the Ca 2ϩ selective pore-forming unit of the Ca 2ϩ release-activated Ca 2ϩ channel (3). Stromal interaction molecule 1 (STIM1) serves as a Ca 2ϩ sensor in the endoplasmic reticulum/sarcoplasmic reticulum (SR), clustering proximal to the plasma membrane to activate Orai1 (4) and TRPC channel(s) (5) when Ca 2ϩ stores are depleted.…”

mentioning

confidence: 99%

Transient Receptor Potential Canonical (TRPC)/Orai1-dependent Store-operated Ca2+ Channels

Sabourin

Bartoli

Antigny

et al. 2016

Journal of Biological Chemistry

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Store-operated Ca2؉ entry (SOCE) has emerged as an important mechanism in cardiac pathology. However, the signals that up-regulate SOCE in the heart remain unexplored. Clinical trials have emphasized the beneficial role of mineralocorticoid receptor (MR) signaling blockade in heart failure and associated arrhythmias. Accumulated evidence suggests that the mineralocorticoid hormone aldosterone, through activation of its receptor, MR, might be a key regulator of Ca 2؉ influx in cardiomyocytes. We thus assessed whether and how SOCE involving transient receptor potential canonical (TRPC) and Orai1 channels are regulated by aldosterone/MR in neonatal rat ventricular cardiomyocytes. Molecular screening using qRT-PCR and Western blotting demonstrated that aldosterone treatment for 24 h specifically increased the mRNA and/or protein levels of Orai1, TRPC1, -C4, -C5, and stromal interaction molecule 1 through MR activation. These effects were correlated with a specific enhancement of SOCE activities sensitive to store-operated channel inhibitors (SKF-96365 and BTP2) and to a potent Orai1 blocker (S66) and were prevented by TRPC1, -C4, and Orai1 dominant negative mutants or TRPC5 siRNA. A mechanistic approach showed that up-regulation of serum-and glucocorticoid-regulated kinase 1 mRNA expression by aldosterone is involved in enhanced SOCE. Functionally, 24-h aldosterone-enhanced SOCE is associated with increased diastolic [Ca 2؉ ] i , which is blunted by store-operated channel inhibitors. Our study provides the first evidence that aldosterone promotes TRPC1-, -C4-, -C5-, and Orai1-mediated SOCE in cardiomyocytes through an MR and serum-and glucocorticoid-regulated kinase 1 pathway.The last discovered Ca 2ϩ channel family, transient receptor potential canonical (TRPC) 2 and Orai1 channels, is widely expressed, but the role of these channels and the modulation of their expression are not completely understood. Notably, the dysregulation of these important mediators of Ca 2ϩ -dependent signal transduction has been involved in a broad range of human diseases such as adenocarcinomas, type 2 diabetes and diabetic nephropathy, human proteinuric kidney disease focal and segmental glomerulosclerosis, severe immunodeficiency, congenital myopathy, chronic pulmonary disease, and ectodermal dysplasia (1, 2). Although predominantly thought of in the context of non-excitable cells, store-operated Ca 2ϩ entry (SOCE) by store-operated channels (SOCs) has recently emerged as a potential mechanism to alter Ca 2ϩ in the diseased cardiomyocyte. Although still under debate, the prime candidate proteins for SOCs encompass the TRPC channel(s) as non-selective cation channels as well as Orai1, the Ca 2ϩ selective pore-forming unit of the Ca 2ϩ release-activated Ca 2ϩ channel (3). Stromal interaction molecule 1 (STIM1) serves as a Ca 2ϩ sensor in the endoplasmic reticulum/sarcoplasmic reticulum (SR), clustering proximal to the plasma membrane to activate Orai1 (4) and TRPC channel(s) (5) when Ca 2ϩ stores are depleted. The seven isoforms of the T...

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“…This is usually referred to as the "store-operated calcium entry" (or SOCE) model [105]. The link between the emptying of the intracellular stores (and indeed their specific identity) and the opening of the plasma membrane calcium channels remains to be characterized in details although the contribution of endoplasmic reticulum-associated Stim-1 and plasma membrane-associated Orai proteins (forming the calcium channels termed I CRAC ) appears highly likely [106][107][108][109].…”

Section: Downstream Effector Pathwaysmentioning

confidence: 99%

Signalling in Neutrophils: A Retro Look

Naccache

2013

ISRN Physiology

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This review presents a summary of signalling events related to the activation of human polymorphonuclear neutrophils by a variety of soluble and particulate agonists. It is not intended as a comprehensive review of this vast field or as a presentation of the multiple new aspects of neutrophil functions that are being documented at an ever faster rate. Its aim is rather to focus on multiple aspects of major signalling pathways that, in the view of this reviewer, are currently shadowed by present trends and to provide the core evidence for their implication and the limitations of our present knowledge. More specifically, this review starts with cell surface receptors and some of their functional and biological properties and then moves on to downstream transducers (G proteins) and effectors (the phosphoinositide, tyrosine kinases, and cyclic nucleotide pathways). Classical second messengers (calcium, protein kinase C, polyphosphoinositides, and cyclic nucleotides) are emphasized. It is hoped that this presentation will not only remind present-day investigators of the central role these pathways play in the regulation of the functional responsiveness of neutrophils, but that it will also highlight some of the areas deserving additional investigation.

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Store-Operated Ca2+ Entry

Cited by 48 publications

References 263 publications

Calcium signaling in pancreatic β-cells in health and in Type 2 diabetes

Calcium signaling in pancreatic β-cells in health and in Type 2 diabetes

Transient Receptor Potential Canonical (TRPC)/Orai1-dependent Store-operated Ca2+ Channels

Signalling in Neutrophils: A Retro Look

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