Fetal hemorrhage and platelet dysfunction in SLP-76–deficient mice

摘要: The adapter protein SLP-76 is expressed in T lymphocytes and hematopoietic cells of the myeloid lineage, known to be a substrate tyrosine kinases that are activated after ligation T-cell antigen receptor. Transient overexpression line potentiates transcriptional activation receptor ligation, while loss expression abrogates several receptor–dependent signaling pathways. Mutant mice lack manifest severe block at an early stage thymocyte development, implicating events promote maturation. While it clear plays key role development lymphocytes, relatively little understood regarding its transducing signals initiated other cell types. In this report, we describe fetal hemorrhage perinatal mortality SLP-76–deficient mice. Although megakaryocyte platelet proceeds normally absence SLP-76, collagen-induced aggregation granule release markedly impaired. Furthermore, treatment platelets with collagen fails elicit phosphorylation phospholipase C-γ2 (PLC-γ2), suggesting functions upstream PLC-γ2 activation. These data provide one potential mechanism for observed reveal required optimal receptor-mediated signal transduction as well lymphocytes.