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|Title:||T cell receptor-mediated signaling induces GRP78 expression in T cells: The implications in maintaining T cell viability|
|Citation:||Biochemical and Biophysical Research Communications, 2008; 371(4):762-766|
|Publisher:||Academic Press Inc|
|Shinichi Takano, Takashi Ando, Nobuhiko Hiramatsu, Asuka Kanayama, Shinya Maekawa, Yuko Ohnuma, Nobuyuki Enomoto, Hideoki Ogawa, Adrienne W. Paton, James C. Paton, Masanori Kitamura and Atsuhito Nakao|
|Abstract:||The 78-kDa glucose-regulated protein (GRP78) is an important molecular chaperone in the endoplasmic reticulum (ER) induced by various stresses. This study showed that stimulation with anti-CD3 mAb, PMA plus ionomycin, or an antigen increased the levels of GRP78 mRNA in primary T cells, which was inhibited by Ca2+ chelators EGTA and BAPTA-AM and by an inhibitor of calcineurin FK506. In addition, the specific knockdown of GRP78 protein expression induced apoptosis in mouse EL-4 T cell line associated with CHOP induction and caspase-3 activation. Furthermore, overexpression of GRP78 inhibited PMA/ionomycin-induced cell death in EL-4 cells. Collectively, GRP78 expression is induced by TCR activation via a Ca2+-dependent pathway and may play a critical role in maintaining T cell viability in the steady and TCR-activated states. These results suggest a novel regulatory mechanism and an essential function of GRP78 in T cells.|
|Keywords:||GRP78/BiP; T cells; T cell receptor; Apoptosis|
|Description:||Copyright © 2008 Elsevier B.V. All rights reserved. ScienceDirect® is a registered trademark of Elsevier B.V.|
|Appears in Collections:||Molecular and Biomedical Science publications|
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