Opposing regulation of B cell receptor‐induced activation of mitogen‐activated protein kinases by CD45

FEBS Letters

Nebreda, Angel R.¹  Woodgett, James R.²  Arimura, Yutaka³  Katagiri, Tatsuo³  Mizuno, Kazuya³  Yakura, Hidetaka³  Mitomo, Katsuyuki³  Ogimoto, Mami³ 

[1] European Molecular Biology Laboratory, 69117 Heidelberg, Germany;Ontario Cancer Institute, Toronto, Ont., Canada M5G 2M9;Department of Immunology and Signal Transduction, Tokyo Metropolitan Institute for Neuroscience, Tokyo Metropolitan Organization for Medical Research, 2-6 Musashidai, Fuchu, Tokyo 183-8526, Japan

关键词: B lymphocyte;    CD45;    Mitogen-activated protein kinase;    Protein tyrosine phosphatase;    Signal transduction;    BCR;    B cell antigen receptor;    ERK;    extracellular signal-regulated kinase;    JNK;    c-Jun NH2-terminal kinase;    MAPK;    mitogen-activated protein kinase;   

DOI  :  10.1016/S0014-5793(00)02416-9

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

In this study, we examined the contribution made by CD45 to B cell antigen receptor (BCR)-induced activation of mitogen-activated protein kinase (MAPK) family members. We found that CD45 negatively regulated BCR-induced c-Jun NH₂-terminal kinase (JNK) and p38 activation in immature WEHI-231 cells, whereas in mature BAL-17 cells, CD45 positively regulated JNK and p38 activation and negatively regulated extracellular signal-regulated kinase activity. Furthermore, cooperative action of JNK and p38 dictated BCR-induced inhibition of growth. Thus, CD45 appears to differentially regulate BCR-induced activation of MAPK members, and can exert opposing effects on JNK and p38 in different cellular milieu, controlling the B cell fate.

【 授权许可】

Unknown