Results demonstrated that loss of ADAP restricted to the megakaryocytic lineage has no impact on other hematopoietic cells causes thrombocytopenia and reduced plasma levels of PF4 and TGF-beta1 impairs CLEC-2-mediated platelet activation in vitro and results in enhanced experimental autoimmune encephalomyelitis severity.
Adap(-/-) mice have moderate thrombocytopenia and smaller platelets. Adap(-/-) platelets had a shorter life span than controlss. Cultured ADAP(-) BM-derived MKs had reduced spreading on extracellular matrix proteins and beta1 integrin activation impaired podosome formation and defective polarization of the demarcation membrane system. ADAP has an unspecified role in the process of MK polarization and platelet biogene...
ADAP regulates CD8 T cell differentiation events following acute pathogen challenge that are critical for the formation and selected functions of TRM cells in nonlymphoid tissues.
The results indicate that ADAP dampens naive CD8 T cell responses to lymphopenia and IL-15 and they demonstrate a novel Ag-independent function for ADAP in the suppression of memory phenotype CD8 T cell generation.
Data (including data from studies in knockout/transgenic mice) suggest that ADAP regulates positive feedback loop of TGFbeta1 production and TGFbeta1-induced CD103 expression in CD8+ T-lymphocytes and protects against influenza H5N1 virus infection.
we demonstrate that loss of ADAP promotes resistance of experimental autoimmune encephalomyelitis in mice likely by trapping encephalitogenic T cells in the peripheral lymph nodes on LYVE-1+ lymphatic structures.
SLP-76 and ADAP are involved in E-selectin-mediated integrin activation and neutrophil recruitment to inflamed kidneys which may underlie the development of life-threatening ischemia-reperfusion-induced acute kidney injury in humans.
ADAP is an essential component of alphaIIbbeta3-mediated platelet mechanotransduction that promotes F-actin assembly and enables platelet spreading and thrombus stabilization under fluid shear stress.
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