Activation of RasGRP3 by phosphorylation of Thr-133 is required for B cell receptor-mediated Ras activation

Yuichi Aiba, Masatsugu Oh-Hora, Shigeki Kiyonaka, Yayoi Kimura, Atsushi Hijikata, Yasuo Mori, Tomohiro Kurosaki

研究成果: Contribution to journalArticle査読

66 被引用数 (Scopus)

抄録

The Ras signaling pathway plays a critical role in B lymphocyte development and activation, but its activation mechanism has not been well understood. At least one mode of Ras regulation in B cells involves a Ras-guanyl nucleotide exchange factor, RasGRP3. We demonstrate here that RasGRP3 undergoes phosphorylation at Thr-133 upon B cell receptor cross-linking, thereby resulting in its activation. Deletion of phospholipase C-γ2 or pharmacological interference with conventional PKCs resulted in marked reduction in both Thr-133 phosphorylation and Ras activation. Moreover, mutation of Thr-133 in RasGRP3 alone severely impaired its ability to activate Ras in B cell receptor signaling. Hence, our data suggest that PKC, after being activated by diacylglycerol, phosphorylates RasGRP3, thereby contributing to its full activation.

本文言語英語
ページ(範囲)16612-16617
ページ数6
ジャーナルProceedings of the National Academy of Sciences of the United States of America
101
47
DOI
出版ステータス出版済み - 11 23 2004
外部発表はい

All Science Journal Classification (ASJC) codes

  • 一般

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