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. Author manuscript; available in PMC: 2014 Jun 1.
Published in final edited form as: J Mol Cell Cardiol. 2013 Feb 13;59:1–10. doi: 10.1016/j.yjmcc.2013.01.018

Figure 6. Inhibition of the Ubiquitin-Proteasome System (UPS) abrogates the anti-apoptotic effects of FAT10.

Figure 6

A. Western blots showing levels of p53, BCL2 and BAX proteins in cardiac myocytes transduced with recombinant lentiviruses expressing FAT10 before and after treatment with MG132 for 4 h under normoxic conditions as well as before and after exposure to H/R. β-actin was used as a control for loading conditions. Over-expression of FAT10 is associated with reduced p53 and BAX levels and increased BCL2 level. Treatment with MG132 attenuates the molecular anti-apoptotic effects observed upon over-expression of FAT10.

B. Quantitative analysis of p53, BCL2 and BAX proteins levels in the experimental groups. *p<0.05 under normoxic, and #p<0.05 vs. normoxic groups.

C. qPCR analysis of miR-34a level in the experimental group. Data were shown as Mean ± SEM in 3 tests from different experiments for each group. *p<0.05 vs normoxic group.

D. A proposed mechanism for the anti-apoptotic role of FAT10 in NRCM. FAT10 through fatylation and UPS-mediated degradation reduced level of p53 and its trans-regulated miR, miR34-a, which in turn results in increased expression of anti-apoptotic protein BCL2 and reduced apoptosis.