Title : Bcl-2 and Bcl-xL suppress glucose signaling in pancreatic β-cells.

Pub. Date : 2013 Jan

PMID : 22933114






7 Functional Relationships(s)
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Protein Name
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1 Bcl-2 and Bcl-xL suppress glucose signaling in pancreatic beta-cells. Glucose BCL2-like 1 Mus musculus
2 In this study, we demonstrate that chemical and genetic loss-of-function of antiapoptotic Bcl-2 and Bcl-x(L) significantly augments glucose-dependent metabolic and Ca(2+) signals in primary pancreatic beta-cells. Glucose BCL2-like 1 Mus musculus
3 Antagonism of Bcl-2/Bcl-x(L) by two distinct small-molecule compounds rapidly hyperpolarized beta-cell mitochondria, increased cytosolic Ca(2+), and stimulated insulin release via the ATP-dependent pathway in beta-cell under substimulatory glucose conditions. Glucose BCL2-like 1 Mus musculus
4 Inducible deletion of Bcl-x(L) in adult mouse beta-cells also increased glucose-stimulated NAD(P)H and Ca(2+) responses and resulted in an improvement of in vivo glucose tolerance in the conditional Bcl-x(L) knockout animals. Glucose BCL2-like 1 Mus musculus
5 Inducible deletion of Bcl-x(L) in adult mouse beta-cells also increased glucose-stimulated NAD(P)H and Ca(2+) responses and resulted in an improvement of in vivo glucose tolerance in the conditional Bcl-x(L) knockout animals. Glucose BCL2-like 1 Mus musculus
6 Inducible deletion of Bcl-x(L) in adult mouse beta-cells also increased glucose-stimulated NAD(P)H and Ca(2+) responses and resulted in an improvement of in vivo glucose tolerance in the conditional Bcl-x(L) knockout animals. Glucose BCL2-like 1 Mus musculus
7 Inducible deletion of Bcl-x(L) in adult mouse beta-cells also increased glucose-stimulated NAD(P)H and Ca(2+) responses and resulted in an improvement of in vivo glucose tolerance in the conditional Bcl-x(L) knockout animals. Glucose BCL2-like 1 Mus musculus