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Blood, 1 March 2008, Vol. 111, No. 5, pp. 2685-2692. Prepublished online as a Blood First Edition Paper on November 29, 2007; DOI 10.1182/blood-2006-12-062265.
IMMUNOBIOLOGY ZAP-70 enhances IgM signaling independent of its kinase activity in chronic lymphocytic leukemia1 Moores UCSD Cancer Center, University of California, San Diego; 2 Chronic Lymphocytic Leukemia (CLL) Research Consortium, San Diego, CA; 3 Department of Cell Signaling Research, BD PharMingen, San Diego, CA; and 4 Department of Medicine, Howard Hughes Medical Institute, University of California, San Francisco
We transduced chronic lymphocytic leukemia (CLL) cells lacking ZAP-70 with vectors encoding ZAP-70 or various mutant forms of ZAP-70 and monitored the response of transduced CLL cells to treatment with F(ab)2 anti-IgM (anti-µ). CLL cells made to express ZAP-70, a kinase-defective ZAP-70 (ZAP-70-KA369), or a ZAP-70 unable to bind c-Cbl (ZAP-YF292) experienced greater intracellular calcium flux and had greater increases in the levels of phosphorylated p72Syk, B-cell linker protein (BLNK), and phospholipase C-
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