Transient activation of the c-Jun N-terminal kinase (JNK) activity by ligation of the tetraspan CD53 antigen in different cell types

被引:17
作者
Yunta, M
Oliva, JL
Barcia, R
Horejsi, V
Angelisova, P
Lazo, PA
机构
[1] Univ Salamanca, CSIC, Ctr Invest Canc, Inst Biol Mol & Celular Canc, E-37007 Salamanca, Spain
[2] Inst Salud Carlos III, Ctr Nacl Biol Fundamental, Unidad Biol Celular, Majadahonda, Spain
[3] Acad Sci Czech Republ, Inst Mol Genet, Prague, Czech Republic
来源
EUROPEAN JOURNAL OF BIOCHEMISTRY | 2002年 / 269卷 / 03期
关键词
CD53; JNK; Jun kinase; tetraspan antigen; signal transduction;
D O I
10.1046/j.0014-2956.2001.02741.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The CD53 antigen is a member of the tetraspanin membrane protein family that is expressed in the lymphoid-myeloid lineage. We have studied the implication of CD53 antigen in signal transduction by determining the effect of its ligation on the c-Jun N-terminal kinase (JNK) in different cell types. Ligation of the rat or human CD53 antigen induces a three-to fourfold transient activation of JNK activity that peaks at 3-5 min. The effect was detected by assaying the endogenous or exogenous (transfected) JNK activity. The JNK response was detected in IR938F cells, a rat B-cell lymphoma, and in Jurkat cells derived from a human T-cell lymphoma. This JNK activation was not mediated by the vav oncogene, and CD53 does not cooperate with CD3 for vav activation. A similar JNK activation was also detected in a human renal carcinoma cell title that was transiently transfected with the human CD53 cDNA to mimic the CD53 ectopic expression in carcinomas. In stable CD53-transfected cells it stimulated Jun-dependent transcriptional activity. We conclude that parts of the cell responses modulated by the CD53 are mediated by JNK activation, and this activation is independent of the different protein interactions that the CD53 protein has oil specific cell types.
引用
收藏
页码:1012 / 1021
页数:10
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