منابع مشابه
CalDAG-GEFI Deficiency Reduces Atherosclerotic Lesion Development in Mice.
OBJECTIVE Platelets are important for the development and progression of atherosclerotic lesions. However, relatively little is known about the contribution of platelet signaling to this pathological process. Our recent work identified 2 independent, yet synergistic, signaling pathways that lead to the activation of the small GTPase Rap1; one mediated by the guanine nucleotide exchange factor, ...
متن کاملMice lacking the signaling molecule CalDAG-GEFI represent a model for leukocyte adhesion deficiency type III.
Single gene mutations in beta integrins can account for functional defects of individual cells of the hematopoietic system. In humans, mutations in beta(2) integrin lead to leukocyte adhesion deficiency (LAD) syndrome and mutations in beta(3) integrin cause the bleeding disorder Glanzmann thrombasthenia. However, multiple defects in blood cells involving various beta integrins (beta(1), beta(2)...
متن کاملCalDAG-GEFI deficiency protects mice in a novel model of Fcγ RIIA-mediated thrombosis and thrombocytopenia.
Platelet activation via Fcγ receptor IIA (FcγRIIA) is a critical event in immune-mediated thrombocytopenia and thrombosis syndromes (ITT). We recently identified signaling by the guanine nucleotide exchange factor CalDAG-GEFI and the adenosine diphosphate receptor P2Y12 as independent pathways leading to Rap1 small GTPase activation and platelet aggregation. Here, we evaluated the contribution ...
متن کاملIntegrin-independent role of CalDAG-GEFI in neutrophil chemotaxis.
Chemotaxis and integrin activation are essential processes for neutrophil transmigration in response to injury. CalDAG-GEFI plays a key role in the activation of beta1, beta2, and beta3 integrins in platelets and neutrophils by exchanging a GDP for a GTP on Rap1. Here, we explored the role of CalDAG-GEFI and Rap1b in integrin-independent neutrophil chemotaxis. In a transwell assay, CalDAG-GEFI-...
متن کاملIdentification of a severe bleeding disorder in humans caused by a mutation in CalDAG-GEFI
1271 INSIGHTS | The Journal of Experimental Medicine In this issue, Canault et al. report for the first time a point mutation in the RAS guanyl-releasing protein 2 (RASGRP2) gene that results in a severe bleeding defect in humans. The study of inherited platelet disorders has shed light on the molecular mechanisms of physiologic thrombosis and hemostasis and led to the development of several th...
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ژورنال
عنوان ژورنال: Blood
سال: 2016
ISSN: 0006-4971,1528-0020
DOI: 10.1182/blood-2016-07-719906