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pubmed-article:9547347pubmed:abstractTextPaired immunoglobulin-like receptor B (PIR-B) (p91) molecule has been proposed to function as an inhibitory receptor in B cells and myeloid lineage cells. We demonstrate here that the cytoplasmic region of PIR-B is capable of inhibiting B cell activation. Mutational analysis of five cytoplasmic tyrosines indicate that tyrosine 771 in the motif VxYxxL plays the most crucial role in mediating the inhibitory signal. PIR-B-mediated inhibition was markedly reduced in the SH2-containing protein tyrosine phosphatases SHP-1 and SHP-2 double-deficient DT40 B cells, whereas this inhibition was unaffected in the inositol polyphosphate 5'-phosphatase SHIP-deficient cells. These data demonstrate that PIR-B can negatively regulate B cell receptor activation and that this PIR-B-mediated inhibition requires redundant functions of SHP-1 and SHP-2.lld:pubmed
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pubmed-article:9547347pubmed:articleTitleRequirement of SH2-containing protein tyrosine phosphatases SHP-1 and SHP-2 for paired immunoglobulin-like receptor B (PIR-B)-mediated inhibitory signal.lld:pubmed
pubmed-article:9547347pubmed:affiliationDepartment of Molecular Genetics, Institute for Liver Research, Kansai Medical University, Moriguchi 570, Japan.lld:pubmed
pubmed-article:9547347pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:9547347pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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