Ontology highlight
ABSTRACT: Abstract
Rubicon (RUN domain Beclin-1-interacting and cysteine-rich-containing protein) is a negative regulator of autophagy in nucleated cells; however, its role in platelets is unstudied. Here, we identify an autophagy-independent role for Rubicon in arterial thrombosis. Mice with a platelet/megakaryocyte-specific deletion of Rubicon (RUBCN-/-) showed normal circulating platelet counts, with a slight increase in platelet size. The basal levels of autophagy-related, vesicle-elongation proteins (ie, ATG5, ATG7, syntaxin 17, LC3, and Rab7) were unaffected, and there was no disruption in canonical platelet signaling pathways upon activation. Platelet secretion from all 3 granule classes remained intact. Aggregation/Agglutination in response to thrombin, convulxin, or botrocetin was u
SUBMITTER: Alfar HR
PROVIDER: S-EPMC12946915 | biostudies-literature | 2026 Feb
REPOSITORIES: biostudies-literature