Articles by G. Stefano Brigidi in JoVE
Detektering av protein palmitoylering i odlade hippocampus neuroner genom immunprecipitation och Acyl-Biotin Exchange (ABE) G. Stefano Brigidi1, Shernaz X Bamji1 1Department of Cellular and Physiological Sciences, Brain Research Centre, University of British Columbia Den reversibla tillägg av palmitat till proteiner är en viktig reglerare av intracellulärt protein människohandel. Detta är av särskilt intresse i neuroner där många synaptiska proteiner palmitoylerad. Vi använder en enkel biokemisk metod för att detektera palmitoylerade proteiner i odlade neuroner, som kan anpassas för flera celltyper och vävnader.
Other articles by G. Stefano Brigidi on PubMed
Cadherin-catenin Adhesion Complexes at the Synapse Current Opinion in Neurobiology. Apr, 2011 | Pubmed ID: 21255999 Classic cadherins function as key organizers during the formation and remodeling of synapses in the vertebrate central nervous system. Cadherins are Ca2+-dependent homophilic adhesion molecules whose adhesive strength can be regulated by conformational changes, through cadherin's association with intracellular binding proteins, and by the regulation of cadherin turnover and internalization. In this mini-review, we will highlight recent studies on the role of cadherins and their associated partners in regulating synaptic architecture. Moreover, we will discuss molecular mechanisms underlying cadherin turnover and the subsequent impact on synaptic connections.
Hyperinsulinemia Drives Diet-induced Obesity Independently of Brain Insulin Production Cell Metabolism. Dec, 2012 | Pubmed ID: 23217255 Hyperinsulinemia is associated with obesity and pancreatic islet hyperplasia, but whether insulin causes these phenomena or is a compensatory response has remained unsettled for decades. We examined the role of insulin hypersecretion in diet-induced obesity by varying the pancreas-specific Ins1 gene dosage in mice lacking Ins2 gene expression in the pancreas, thymus, and brain. Age-dependent increases in fasting insulin and Î² cell mass wereÂ absent in Ins1(+/-):Ins2(-/-) mice fed a high-fat diet when compared to Ins1(+/+):Ins2(-/-) littermate controls. Remarkably, Ins1(+/-):Ins2(-/-) mice were completely protected from diet-induced obesity. Genetic prevention of chronic hyperinsulinemia in this model reprogrammed white adipose tissue to express uncoupling protein 1 and increase energy expenditure. Normalization of adipocyte size and activation of energy expenditure genes in white adipose tissue was associated with reduced inflammation, reduced fatty acid spillover, and reduced hepatic steatosis. Thus, we provide genetic evidence that pathological circulating hyperinsulinemia drives diet-induced obesity and its complications.