Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/50773
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Type: Journal article
Title: T cell receptor-mediated signaling induces GRP78 expression in T cells: The implications in maintaining T cell viability
Author: Takano, S.
Ando, T.
Hiramatsu, N.
Kanayama, A.
Maekawa, S.
Ohnuma, Y.
Enomoto, N.
Ogawa, H.
Paton, A.
Paton, J.
Kitamura, M.
Nakao, A.
Citation: Biochemical and Biophysical Research Communications, 2008; 371(4):762-766
Publisher: Academic Press Inc
Issue Date: 2008
ISSN: 0006-291X
1090-2104
Statement of
Responsibility: 
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.
RMID: 0020080889
DOI: 10.1016/j.bbrc.2008.04.132
Appears in Collections:Molecular and Biomedical Science publications

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