Bcl-2 and Bcl-xL Suppress Glucose Signaling in Pancreatic β-Cells

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FIG. 8.
FIG. 8.

Effect of Bcl antagonism in Bax, Bak, and Bcl-xL–deficient islet cells. A: Percentage of islet cells responding to Bcl antagonism in preparations from Bax−/− (left), Bak−/− (right), and their wild-type control mice (n = 3 mice). Data are mean ± SEM. Basal glucose was 3 mmol/L in all experiments. B: Western blot demonstrating global Bak deficiency and islet specific Bax knockout in tamoxifen-injected Bak−/−:Baxflox/flox:Pdx1-CreER (Bax-Bak βDKO) mice relative to tamoxifen-injected Bak−/−:Baxflox/flox and C57BL6/J (C57) mice. C: Bax protein levels were reduced by 85% in Bax-Bak βDKO islets (n = 6; **P < 0.001 vs. Bak−/−:Baxflox/flox). D: Comparable Bcl inhibitor-induced Ca2+ responses in groups of Bak−/−Baxflox/flox and Bax-Bak βDKO islet cells. E: Percentage of Bak-Bax βDKO and Bak−/−:Baxflox/flox islet-cells responding to Bcl inhibition (n = 3 mice of each genotype). (A high-quality color representation of this figure is available in the online issue.)

This Article

  1. Diabetes vol. 62 no. 1 170-182