fig1

Ser9 phosphorylation of GSK-3β promotes aging in the heart through suppression of autophagy

Figure 1. GSK-3β and GSK-3α in the aged heart. (A) Immunoblots of phospho(S9)-GSK-3β, GSK-3β, phospho(S21)-GSK-3α, GSK-3α, β-catenin, myeloid cell leukemia 1 (Mcl-1), and tubulin in left ventricular homogenates from WT and homozygous GSK-3βS9A knock-in mice (βKI) at 6 and 24 months (M) of age. The results of two experiments (out of four) are shown. (B) Relative band density of pGSK-3β/GSK-3β. *P < 0.05 vs. WT 6M (WT6). WT24, WT 24M; βKI6, βKI 6M; βKI24, βKI 24M. (C) Relative band density of pGSK-3α/GSK-3α. (D) Relative band density of β-catenin/tubulin. *P < 0.05 vs. WT6, #P < 0.05 vs. WT24. (E) Relative band density of phospho-β-catenine/β-catenin. *P < 0.05 vs. WT6, #P < 0.05 vs. WT24. (F) Relative band density of Mcl-1/tubulin. *P < 0.05 vs. WT6, #P < 0.05 vs. WT24. In (B-F), n = 4 in each group. WT: Wild type.

The Journal of Cardiovascular Aging

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