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Cell Calcium. 2015 Oct;58(4):368-75. doi: 10.1016/j.ceca.2015.04.004. Epub 2015 Apr 22.

Store-operated Ca²⁺-entry and adenylyl cyclase.

Author information

1
Department of Pharmacology, University of Cambridge, Cambridge CB2 1PD, United Kingdom. Electronic address: dmfc2@cam.ac.uk.

Abstract

One of the longest-standing effects of SOCE is in its selective regulation of Ca(2+)-sensitive adenylyl cyclase (AC) activity in non-excitable cells. Remarkably it was this source of Ca(2+) (SOCE) rather than the apparent magnitude of the Ca(2+)-rise that conferred AC responsiveness. The molecular basis for this dependence is now resolved in the case of adenylyl cyclase 8 (AC8). Sensors for Ca(2+) and cAMP targeted to ACs have been particularly useful in dissecting the influences upon and composition of what turn out to be signalling microdomains centred on ACs. A number of physiological processes depend on the regulation by SOCE of ACs, but the issue is under-studied. Here I will expand on these topics and point to some immediate unresolved questions.

KEYWORDS:

Adenylyl cyclase; Calcium; Calmodulin; Orai1; SOCE; Stim1

PMID:
25978874
DOI:
10.1016/j.ceca.2015.04.004
[Indexed for MEDLINE]
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