Article
CD22 EXON 12 deletion as a pathogenic mechanism of human B-precursor leukemia
14 Sept 2010
Abstract excerpt
Here, we report that primary leukemic cells from infants with newly diagnosed B-precursor leukemia express a truncated and functionally defective CD22 coreceptor protein that is unable to transmit apoptotic signals because it lacks most of the intracellular domain, including the key regulatory signal transduction elements and all of the cytoplasmic tyrosine residues. Expression of this structurally and...
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