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Dual role of proapoptotic BAD in insulin secretion and beta cell survival
Area: Diabetes
Genetic evidence of a physiologic role for the proapoptotic BCL-2 family member BAD in glucose-stimulated insulin secretion by beta cells was found by Nika N. Danial and colleagues from the Harvard Medical School's Dana-Farber Cancer Institute (USA).
BAD usually resides in a glucokinase-containing complex that regulates glucose-driven mitochondrial respiration. The novel function turns out to be specifically dependent upon the phosphorylation of its BH3 sequence, an essential death domain.
The scientists analysed the pharmacologic relevance of phosphorylated BAD BH3 with cell-permeable, hydrocarbon-stapled BAD BH3 helices that target glucokinase, restore glucose-driven mitochondrial respiration and correct the insulin secretory response in BAD-deficient islets. Using this approach they discovered an alternative target and function for the BAD BH3 domain. The phosphorylated BAD BH3 selectively restores beta cell functions and thus bears great therapeutic potential. BAD also regulates the physiologic adaptation of beta cell mass during a high-fat diet.
Related antibodies on antibodies-online.com:
BH3 interacting domain death antagonist (BID)
Antibodies for the research area diabetes: »Show antibodies
14.05.2008 | Anna Lena Marwedel 
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