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Tuning store-operated calcium entry to modulate Ca2+-dependent physiological processes.
Biochim Biophys Acta Mol Cell Res. 2019 07; 1866(7):1037-1045.BB

Abstract

The intracellular calcium signaling processes are tightly regulated to ensure the generation of calcium signals with the specific spatiotemporal characteristics required for regulating various cell functions. Compartmentalization of the molecular components involved in the generation of these signals at discrete intracellular sites ensures the signaling specificity and transduction fidelity of the signal for regulating downstream effector processes. Store-operated calcium entry (SOCE) is ubiquitously present in cells and is critical for essential cell functions in a variety of tissues. SOCE is mediated via plasma membrane Ca2+ channels that are activated when luminal [Ca2+] of the endoplasmic reticulum ([Ca2+]ER) is decreased. The ER-resident stromal interaction molecules, STIM1 and STIM2, respond to decreases in [Ca2+]ER by undergoing conformational changes that cause them to aggregate at the cell periphery in ER-plasma membrane (ER-PM) junctions. At these sites, STIM proteins recruit Orai1 channels and trigger their activation. Importantly, the two STIM proteins concertedly modulate Orai1 function as well as the sensitivity of SOCE to ER-Ca2+ store depletion. Another family of plasma membrane Ca2+ channels, known as the Transient Receptor Potential Canonical (TRPC) channels (TRPC1-7) also contribute to sustained [Ca2+]i elevation. Although Ca2+ signals generated by these channels overlap with those of Orai1, they regulate distinct functions in the cells. Importantly, STIM1 is also required for plasma membrane localization and activation of some TRPCs. In this review, we will discuss various molecular components and factors that govern the activation, regulation and modulation of the Ca2+ signal generated by Ca2+ entry pathways in response to depletion of ER-Ca2+ stores. This article is part of a Special Issue entitled: ECS Meeting edited by Claus Heizmann, Joachim Krebs and Jacques Haiech.

Authors+Show Affiliations

Secretory Physiology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.Secretory Physiology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.Secretory Physiology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.Secretory Physiology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.Secretory Physiology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: indu.ambudkar@nih.gov.

Pub Type(s)

Journal Article
Research Support, N.I.H., Intramural
Review

Language

eng

PubMed ID

30521873

Citation

Ong, Hwei Ling, et al. "Tuning Store-operated Calcium Entry to Modulate Ca2+-dependent Physiological Processes." Biochimica Et Biophysica Acta. Molecular Cell Research, vol. 1866, no. 7, 2019, pp. 1037-1045.
Ong HL, Subedi KP, Son GY, et al. Tuning store-operated calcium entry to modulate Ca2+-dependent physiological processes. Biochim Biophys Acta Mol Cell Res. 2019;1866(7):1037-1045.
Ong, H. L., Subedi, K. P., Son, G. Y., Liu, X., & Ambudkar, I. S. (2019). Tuning store-operated calcium entry to modulate Ca2+-dependent physiological processes. Biochimica Et Biophysica Acta. Molecular Cell Research, 1866(7), 1037-1045. https://doi.org/10.1016/j.bbamcr.2018.11.018
Ong HL, et al. Tuning Store-operated Calcium Entry to Modulate Ca2+-dependent Physiological Processes. Biochim Biophys Acta Mol Cell Res. 2019;1866(7):1037-1045. PubMed PMID: 30521873.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tuning store-operated calcium entry to modulate Ca2+-dependent physiological processes. AU - Ong,Hwei Ling, AU - Subedi,Krishna Prasad, AU - Son,Ga-Yeon, AU - Liu,Xibao, AU - Ambudkar,Indu Suresh, Y1 - 2018/12/03/ PY - 2018/10/12/received PY - 2018/11/28/revised PY - 2018/11/29/accepted PY - 2018/12/7/pubmed PY - 2019/11/26/medline PY - 2018/12/7/entrez SP - 1037 EP - 1045 JF - Biochimica et biophysica acta. Molecular cell research JO - Biochim Biophys Acta Mol Cell Res VL - 1866 IS - 7 N2 - The intracellular calcium signaling processes are tightly regulated to ensure the generation of calcium signals with the specific spatiotemporal characteristics required for regulating various cell functions. Compartmentalization of the molecular components involved in the generation of these signals at discrete intracellular sites ensures the signaling specificity and transduction fidelity of the signal for regulating downstream effector processes. Store-operated calcium entry (SOCE) is ubiquitously present in cells and is critical for essential cell functions in a variety of tissues. SOCE is mediated via plasma membrane Ca2+ channels that are activated when luminal [Ca2+] of the endoplasmic reticulum ([Ca2+]ER) is decreased. The ER-resident stromal interaction molecules, STIM1 and STIM2, respond to decreases in [Ca2+]ER by undergoing conformational changes that cause them to aggregate at the cell periphery in ER-plasma membrane (ER-PM) junctions. At these sites, STIM proteins recruit Orai1 channels and trigger their activation. Importantly, the two STIM proteins concertedly modulate Orai1 function as well as the sensitivity of SOCE to ER-Ca2+ store depletion. Another family of plasma membrane Ca2+ channels, known as the Transient Receptor Potential Canonical (TRPC) channels (TRPC1-7) also contribute to sustained [Ca2+]i elevation. Although Ca2+ signals generated by these channels overlap with those of Orai1, they regulate distinct functions in the cells. Importantly, STIM1 is also required for plasma membrane localization and activation of some TRPCs. In this review, we will discuss various molecular components and factors that govern the activation, regulation and modulation of the Ca2+ signal generated by Ca2+ entry pathways in response to depletion of ER-Ca2+ stores. This article is part of a Special Issue entitled: ECS Meeting edited by Claus Heizmann, Joachim Krebs and Jacques Haiech. SN - 1879-2596 UR - https://www.unboundmedicine.com/medline/citation/30521873/Tuning_store_operated_calcium_entry_to_modulate_Ca2+_dependent_physiological_processes_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0167-4889(18)30522-6 DB - PRIME DP - Unbound Medicine ER -