Insulin releases an intracellular brake and promotes fusion pore expansion to translocate GLUT4 vesicles, and switches vesicle trafficking between distinct exocytic circuits.

Background: GLUT4 glucose transporters are trapped and sequestered intracellularly in adipocytes by TUG. Results: Insulin stimulates TUG cleavage, which separates regions of TUG that bind GLUT4 and Golgi matrix proteins. Cleavage is required for highly insulin-responsive GLUT4 translocation. Conclusion: TUG proteolysis liberates GLUT4 trapped at the Golgi matrix. Significance: Endoproteolytic cleavage is a novel biochemical mechanism for insulin action to regulate glucose uptake.

Capillary malformation-arteriovenous malformation syndrome is an autosomal dominant disorder caused by mutations in the RASA1 gene and characterized by multiple small, round to oval capillary malformations with or without arteriovenous malformations. Ateriovenous malformations occur in up to one-third of patients and may involve the brain and spine. Although making the diagnosis is straightforward in some patients, there are other patients for whom diagnostic criteria may be helpful in their evaluation. Here we review the literature regarding capillary malformation-arteriovenous malformation syndrome, propose diagnostic criteria, and discuss the care of patients with this condition.

Background: TUG controls a specialized membrane trafficking pathway in adipocytes but is widely expressed. Results: TUG converts p97 ATPase hexamers into monomers and controls Golgi membrane dynamics. Conclusion: Localized disassembly of p97 hexamers may control a generalized trafficking pathway in eukaryotic cells. Significance: Understanding how TUG and p97 function provides insight into regulation of both generalized and specialized membrane trafficking.