Co-involvement of the mitochondria and endoplasmic reticulum in cell death induced by the novel ertargeted protein HAP

Cellular & Molecular Biology Letters

Hua Xu¹  Qing Zhou¹  Yi-Peng Qi¹  Xin Liu¹ 

[1] State Key Laboratory of Virology, Section of Molecular Virology, College of Life Sciences, Wuhan University, Wuhan, P. R. China$$

关键词: Apoptosis-inducing protein HAP;    Mitochondria;    Endoplasmic reticulum (ER);    Caspase-12;    Caspase-3;    Mitochondrial membrane potential (Δωm);    Cytochrome c;   

DOI  :  10.2478/s11658-006-0019-1

学科分类：分子生物学，细胞生物学和基因

来源: Uniwersytet Wroclawski * Wydzial Biotechnologii / University of Wroclaw, Faculty of Biotechnology

【 摘 要 】

HAP (a homologue of the ASY/Nogo-B protein), a novel human apoptosis-inducing protein, was found to be identical to RTN3. In an earlier study, we demonstrated that HAP localized exclusively to the endoplasmic reticulum (ER) and that its overexpression could induce cell apoptosis via a depletion of endoplasmic reticulum (ER) Ca2+ stores. In this study, we show that overexpression of HAP causes the activation of caspase-12 and caspase-3. We still detected the collapse of mitochondrial membrane potential (Δωm) and the release of cytochrome c in HAP-overexpressing HeLa cells. All the results indicate that both the mitochondria and the ER are involved in apoptosis caused by HAP overexpression, and suggest that HAP overexpression may initiate an ER overload response (EOR) and bring about the downstream apoptotic events.

【 授权许可】

Unknown