Co-expression of mg29 and ryanodine receptor leads to apoptotic cell death-effect mediated by intracellular Ca2+ release

doi:10.1074/jbc.C400030200

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Papers In Press, published online ahead of print March 23, 2004
J. Biol. Chem, 10.1074/jbc.C400030200
Submitted on January 20, 2004
Revised on March 22, 2004
Accepted on March 23, 2004

Co-expression of mg29 and ryanodine receptor leads to apoptotic cell death-effect mediated by intracellular Ca²+ release

Zui Pan, Yutaka Hirata, Ramakrishnan Y. Nagaraj, Jiying Zhao, Miyuki Nishi, Salim M. Hayek, Manjunatha B. Bhat, Hiroshi Takeshima, and Jianjie Ma

Department of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, Piscataway, NJ 08854

Corresponding Author: maj2{at}umdnj.edu

Perturbation of intracellular Ca²⁺ homeostasis has been shown to regulate the process of cell proliferation and apoptosis. Our previous studies show that mitsugumin29 (MG29), a synaptophysin-related protein localized in the triad junction of skeletal muscle, serves an essential role in muscle Ca²⁺ signaling by regulating the process of store-operated Ca²⁺ entry. Here we report a functional interaction between MG29 and the ryanodine receptor (RyR)/Ca²⁺ release channel. The purified MG29 protein enhances activity of the RyR/Ca²⁺ release channel incorporated into the lipid bilayer membrane. Co-expression of MG29 and RyR in Chinese hamster ovary cells leads to apoptotic cell death resulting from depletion of intracellular Ca²⁺ stores, despite neither protein expression alone exhibits any significant effect on cell viability. In transient expression studies, the presence of RyR in the endoplasmic reticulum leads to retention of MG29 from the plasma membrane into the intracellular organelles. This functional interaction between MG29 and RyR could have important implications in the Ca²⁺ signaling processes of muscle cells. Our data also show that perturbation of intracellular Ca²⁺ homeostasis can serve as a key signal in the initiation of apoptosis.

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