作者: Ryutaro Kajihara , Hitomi Sakamoto , Kano Tanabe , Kazuki Takemoto , Masayoshi Tasaki
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摘要: Crosslinking BCR in the immature B cell line WEHI-231 causes apoptosis. We found that Bcl-xL was degraded by polyubiquitination upon crosslinking and this study explored mechanism controls degradation of Bcl-xL. Ser62 phosphorylated JNK to trigger polyubiquitination, opposed serine/threonine protein phosphatase 6 (PP6) physically associated with show decreased PP6 activity allow phosphorylation CD40 rescues BCR-induced apoptosis, we activation response CD40. Our data suggest is regulated control apoptosis modulating Bcl-xL, which results its degradation.