Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
Volume 1866, Issue 7, Pages 1092-1100Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbamcr.2018.11.007
Keywords
Ca2+ entry; Ca2+ puff; Ca2+ signal; Endoplasmic reticulum; IP3 receptor; Ryanodine receptor; Store-operated Ca2+ entry; STIM
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Funding
- Wellcome Trust [101844]
- Biotechnology and Biological Sciences Research Council UK [BB/P005330/1]
- Department of Science and Technology, Ministry of Science and Technology, India
- DST INSPIRE Fellowship programme
- Infosys
- BBSRC [BB/P005330/1] Funding Source: UKRI
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Inositol 1,4,5-trisphosphate receptors (IP3R) are the most widely expressed intracellular Ca2+ release channels. Their activation by IP3 and Ca2+ allows Ca2+ to pass rapidly from the ER lumen to the cytosol. The resulting increase in cytosolic [Ca2+] may directly regulate cytosolic effectors or fuel Ca2+ uptake by other organelles, while the decrease in ER luminal [Ca2+] stimulates store-operated Ca2+ entry (SOCE). We are close to understanding the structural basis of both IP3R activation, and the interactions between the ER Ca2+-sensor, STIM, and the plasma membrane Ca2+ channel, Orai, that lead to SOCE. IP(3)Rs are the usual means through which extracellular stimuli, through ER Ca2+ release, stimulate SOCE. Here, we review evidence that the IP(3)Rs most likely to respond to IP3 are optimally placed to allow regulation of SOCE. We also consider evidence that IP(3)Rs may regulate SOCE downstream of their ability to deplete ER Ca2+ stores. Finally, we review evidence that IP(3)Rs in the plasma membrane can also directly mediate Ca2+ entry in some cells.
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