RAP1-GTPase signaling and platelet function.
Chapel Hill, United States. In J Mol Med (berl), Jan 2016
Our recent studies demonstrate that the antagonistic balance between the RAP1 regulators, CalDAG-GEFI and RASA3, is critical for the modulation of platelet adhesiveness, both in circulation and at sites of vascular injury.
Update on the inherited platelet disorders.
Philadelphia, United States. In Curr Opin Hematol, Sep 2015
RECENT FINDINGS: The description of novel mechanisms of disease including mutations in PRKACG, in a family with severe macrothrombocytopenia, RUNX1 and FLI1 mutations in patients with inherited mild platelet function disorders and CalDAG-GEFI resulting in a severe platelet bleeding phenotype show that there is still much to be learned from studying families and molecular sequencing of patients with well phenotyped platelet disorders.
Inherited disorders of platelet function: selected updates.
Pessac, France. In J Thromb Haemost, Jun 2015
Next-generation sequencing technology (NGST), mainly exome sequencing, has highlighted genes responsible for defects in platelet secretion (NBEAL2, gray platelet syndrome), procoagulant activity (STIM1, Stormorken syndrome), and activation pathways (RASGRP2, CalDAG-GEFI deficiency and integrin dysfunction; PRKACG, cyclic adenosine monophosphate-dependent protein kinase deficiency).
CalDAG-GEFI and platelet activation.
Philadelphia, United States. In Platelets, 2009
Here, we review recent findings, which (a) identified CalDAG-GEFI (RasGRP2) at the nexus of the rapid Ca(2+)-dependent platelet activation, (b) demonstrated a complex synergy between signaling provided by CalDAG-GEFI, protein kinase C and the Gi-coupled receptor for ADP, P2Y12, and (c) suggested CalDAG-GEFI as a novel target for anti-platelet therapy.
Novel molecules in calcium signaling in platelets.
Philadelphia, United States. In J Thromb Haemost, 2009
Here, we review recent findings, which identified CalDAG-GEFI as a critical Ca2+ sensor that links increases in intracellular Ca2+ to integrin activation, TxA2 formation, and granule release in stimulated platelets.