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Opposing regulation of B cell receptor‐induced activation of mitogen‐activated protein kinases by CD45
Author(s) -
Ogimoto Mami,
Arimura Yutaka,
Katagiri Tatsuo,
Mitomo Katsuyuki,
Woodgett James R.,
Nebreda Angel R.,
Mizuno Kazuya,
Yakura Hidetaka
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)02416-9
Subject(s) - kinase , mapk/erk pathway , p38 mitogen activated protein kinases , microbiology and biotechnology , mitogen activated protein kinase , protein kinase a , breakpoint cluster region , chemistry , b cell receptor , receptor , biology , b cell , biochemistry , antibody , immunology
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 NH 2 ‐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.