Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Blotting, Western
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Cell Line
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Cell Lineage
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Enzyme Activation
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Enzyme Inhibitors / pharmacology
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Flavonoids / pharmacology
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Imidazoles / pharmacology
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JNK Mitogen-Activated Protein Kinases
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Leukocyte Common Antigens / physiology*
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MAP Kinase Signaling System*
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Mice
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Mitogen-Activated Protein Kinases / metabolism
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Pyridines / pharmacology
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Receptors, Antigen, B-Cell / metabolism*
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Time Factors
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Transfection
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p38 Mitogen-Activated Protein Kinases
Substances
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Enzyme Inhibitors
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Flavonoids
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Imidazoles
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Pyridines
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Receptors, Antigen, B-Cell
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JNK Mitogen-Activated Protein Kinases
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Mitogen-Activated Protein Kinases
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p38 Mitogen-Activated Protein Kinases
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Leukocyte Common Antigens
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SB 203580
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2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one