Pore opening mechanism of CRAC channels

Priscilla S.W. Yeung; Megumi Yamashita; Murali Prakriya

doi:10.1016/j.ceca.2016.12.006

Pore opening mechanism of CRAC channels

Priscilla S.W. Yeung, Megumi Yamashita, Murali Prakriya^*

^*Corresponding author for this work

Pharmacology

Research output: Contribution to journal › Review article › peer-review

33 Scopus citations

Abstract

Three decades ago, James W. Putney Jr. conceptualized the idea of store-operated calcium entry (SOCE) to explain how depletion of endoplasmic reticulum (ER) Ca²⁺ stores evokes Ca²⁺ influx across the plasma membrane. Since the publication of this highly influential idea, it is now established that SOCE is universal among non-excitable and probably even many types of excitable cells, and contributes to numerous effector functions impacting immunity, muscle contraction, and brain function. The molecules encoding SOCE, the STIM and Orai proteins, are now known and our understanding of how this pathway is activated in response to ER Ca²⁺ store depletion has advanced significantly. In this review, we summarize the current knowledge of how Orai1 channels are activated by STIM1, focusing on recent work supporting a hydrophobic gating mechanism for the opening of the Orai1 channel pore.

Original language	English (US)
Pages (from-to)	14-19
Number of pages	6
Journal	Cell Calcium
Volume	63
DOIs	https://doi.org/10.1016/j.ceca.2016.12.006
State	Published - May 2017

Funding

The authors would like to thank the members of the laboratory for helpful discussions. The work described in this review was supported by NIH grants NS057499 and GM114210. P. S.-W. Yeung was supported by NIH predoctoral training grant T32GM008382.

Keywords

CRAC channel
Calcium
Orai1
SOCE
STIM1

ASJC Scopus subject areas

Molecular Biology
Physiology
Cell Biology

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10.1016/j.ceca.2016.12.006

Cite this

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title = "Pore opening mechanism of CRAC channels",

abstract = "Three decades ago, James W. Putney Jr. conceptualized the idea of store-operated calcium entry (SOCE) to explain how depletion of endoplasmic reticulum (ER) Ca2+ stores evokes Ca2+ influx across the plasma membrane. Since the publication of this highly influential idea, it is now established that SOCE is universal among non-excitable and probably even many types of excitable cells, and contributes to numerous effector functions impacting immunity, muscle contraction, and brain function. The molecules encoding SOCE, the STIM and Orai proteins, are now known and our understanding of how this pathway is activated in response to ER Ca2+ store depletion has advanced significantly. In this review, we summarize the current knowledge of how Orai1 channels are activated by STIM1, focusing on recent work supporting a hydrophobic gating mechanism for the opening of the Orai1 channel pore.",

keywords = "CRAC channel, Calcium, Orai1, SOCE, STIM1",

author = "Yeung, {Priscilla S.W.} and Megumi Yamashita and Murali Prakriya",

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T1 - Pore opening mechanism of CRAC channels

AU - Yeung, Priscilla S.W.

AU - Yamashita, Megumi

AU - Prakriya, Murali

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N2 - Three decades ago, James W. Putney Jr. conceptualized the idea of store-operated calcium entry (SOCE) to explain how depletion of endoplasmic reticulum (ER) Ca2+ stores evokes Ca2+ influx across the plasma membrane. Since the publication of this highly influential idea, it is now established that SOCE is universal among non-excitable and probably even many types of excitable cells, and contributes to numerous effector functions impacting immunity, muscle contraction, and brain function. The molecules encoding SOCE, the STIM and Orai proteins, are now known and our understanding of how this pathway is activated in response to ER Ca2+ store depletion has advanced significantly. In this review, we summarize the current knowledge of how Orai1 channels are activated by STIM1, focusing on recent work supporting a hydrophobic gating mechanism for the opening of the Orai1 channel pore.

AB - Three decades ago, James W. Putney Jr. conceptualized the idea of store-operated calcium entry (SOCE) to explain how depletion of endoplasmic reticulum (ER) Ca2+ stores evokes Ca2+ influx across the plasma membrane. Since the publication of this highly influential idea, it is now established that SOCE is universal among non-excitable and probably even many types of excitable cells, and contributes to numerous effector functions impacting immunity, muscle contraction, and brain function. The molecules encoding SOCE, the STIM and Orai proteins, are now known and our understanding of how this pathway is activated in response to ER Ca2+ store depletion has advanced significantly. In this review, we summarize the current knowledge of how Orai1 channels are activated by STIM1, focusing on recent work supporting a hydrophobic gating mechanism for the opening of the Orai1 channel pore.

KW - CRAC channel

KW - Calcium

KW - Orai1

KW - SOCE

KW - STIM1

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Pore opening mechanism of CRAC channels

Abstract

Funding

Keywords

ASJC Scopus subject areas

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