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Mimic chronic immune thrombocytopaenia using murine platelet induced model through immunized CD41-knockout mice.
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alphaIIb beta3 antagonist TMV-7/trimucrin prevents thrombosis with causing Fc receptor gamma-chain IIa-mediated thrombocytopenia.
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Kindlin supports platelet GPIIB IIIA activation by interacting with paxillin.
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Platelets from Dok-1-/- mice displayed normal aggregation, activation of integrin alphaIIbbeta3, P-selectin surface expression, and soluble fibrinogen binding. These findings indicate that Dok-1 does not affect "inside-out" platelet signalling.
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platelets clearly support early steps in pulmonary metastasis via GPIIb-dependent formation of platelet-tumor-aggregates
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ITGA2b expression increases in response to immunization, raising the possibility that heterogeneous ITGA2b levels reflect variation in exposure to activation signals.
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Thrombopoietin/MPL signaling confers growth and survival capacity to CD41-positive cells in a mouse model of Evi1 leukemia.
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Direct binding of kindlin-3 to integrin alphaIIbbeta3 is involved in supporting integrin alphaIIbbeta3 activation and integrin alphaIIbbeta3-dependent responses of platelets and consequently contributes significantly to arterial thrombus formation.
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ADAP interacts with talin and kindlin-3 to promote platelet Integrin alphaIIbbeta3 activation and stable fibrinogen binding.
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reduction of talin-beta3 integrin binding affinity results in decelerated alphaIIbbeta3 integrin activation and protection from arterial thrombosis without pathological bleeding
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deficiency of Dok-2 leads to dysregulated integrin alphaIIbbeta3-dependent cytosolic calcium flux and phosphatidylinositol(3,4)P2 accumulation.
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Platelets lacking ERp57 have defective activation of the alphaIIbbeta3 integrin and platelet aggregation. The defect in aggregation was corrected by the addition of exogenous ERp57, implicating surface ERp57 in platelet aggregation.
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Data indicate that Pyk2 is a common signaling effector downstream of both G12/13 and integrin alphaIIbbeta3 signaling, which contributes to thromboxane generation.
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These results identify a novel pathway of integrin alphaIIbbeta3 outside-in signaling and recognize the tyrosine kinase Pyk2 as a major regulator of platelet adhesion and spreading on fibrinogen.
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Here we show that platelet integrin CD41 (alphaIIb), currently thought to only transiently mark fetal hematopoietic stem cells, is expressed on an adult subtype that accumulates with age.
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identified Hic-5 as a novel and specific regulatory factor for thrombin-induced alphaIIbbeta3 activation and subsequent platelet aggregation in mice.
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These results suggested that platelet associated anti-alphaIIbbeta3 antibodies in primary primary immune thrombocytopenia tended to recognize highly restricted regions of alphaIIb with clonality.
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Impaired spreading on fibrinogen and clot retraction with normal levels of alpha(IIb)beta(3) was observed in Lgals1(-/-) platelets, indicating a failure in the "outside-in" signaling through this integrin.
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Glycoprotein IIb/IIIa-targeted microbubbles specifically bind to activated platelets in vitro, allowing real-time molecular imaging of acute arterial thrombosis in a mouse model.
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Data indicate that the inflammatory cytokines TNF-alpha and IL-1 could be key components of the endothelial cell (EC) response and alphaIIb-beta3 integrin in platelets was required for late-phase thrombus stability.