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Title: BLNK required for coupling Syk to PLC gamma 2 and Rac1-JNK in B cells. Author: Ishiai M, Kurosaki M, Pappu R, Okawa K, Ronko I, Fu C, Shibata M, Iwamatsu A, Chan AC, Kurosaki T. Journal: Immunity; 1999 Jan; 10(1):117-25. PubMed ID: 10023776. Abstract: Signaling through the B cell receptor (BCR) is essential for B cell function and development. Despite the key role of Syk in BCR signaling, little is known about the mechanism by which Syk transmits downstream effectors. BLNK (B cell LiNKer protein), a substrate for Syk, is now shown to be essential in activating phospholipase C (PLC)gamma 2 and JNK. The BCR-induced PLC gamma 2 activation, but not the JNK activation, was restored by introduction of PLC gamma 2 membrane-associated form into BLNK-deficient B cells. As JNK activation requires both Rac1 and PLC gamma 2, our results suggest that BLNK regulates the Rac1-JNK pathway, in addition to modulating PLC gamma 2 localization.[Abstract] [Full Text] [Related] [New Search]