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First published online December 21, 2005

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PERKing up Ca²⁺ signalling

The endoplasmic reticulum (ER) is involved in the biosynthesis of secretory proteins and the regulation of the Ca²⁺ signalling events that control their secretion. On p. 153, Shmuel Muallem and co-workers reveal a connection between these two functions by examining Ca²⁺ signalling in secretory cells and in muscle cells (which have a specialized ER called the sarcoplasmic reticulum, SR) from PERK-knockout mice. PERK (pancreatic ER kinase) attenuates protein synthesis in cells in which protein folding is disrupted, thus preventing the development of ER/SR stress. The authors report that, in PERK-null cells, ER/SR stress reduces the rate and efficiency of Ca²⁺ release from the ER/SR and disrupts the integrity of Ca²⁺ signalling complexes. These changes in Ca²⁺ signalling help to explain the decline in secretory cell function in PERK-knockout mice and implicate chronic ER/SR stress in the development of some human conditions. For example, suggest the authors, disruption of Ca²⁺ release by chronic ER/SR stress in pancreatic?-cells and myocytes could contribute to the defects in regulated insulin secretion and cardiac function seen in diabetes.

Related articles in JCS:

ER stress disrupts Ca²⁺-signaling complexes and Ca²⁺ regulation in secretory and muscle cells from PERK-knockout mice

Guojin Huang, Jian Yao, Weizhong Zeng, Yusuke Mizuno, Kristine E. Kamm, James T. Stull, Heather P. Harding, David Ron, and Shmuel Muallem
JCS 2006 119: 153-161. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content