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. 2022 Nov 17;10(2):2204190. doi: 10.1002/advs.202204190

Figure 3.

Figure 3

PPARγ acetylation destabilizes BMAL1 to inhibit adipogenesis. a–c) WT and aKQ primary adipocytes on day 8 of differentiation by vehicle (Veh) or rosiglitazone (Rosi) treatment; a) BODIPY staining showing lipid accumulation; Scale bar, 50 𝜇m. b,c) WB of adipocyte markers and BMAL1 in WT and aKQ adipocytes. d,e) WB of BMAL1 protein (n = 4, 4) and Bmal1 gene expression by qPCR (n = 6, 6) in the eWAT of aKQ mice. Cyclophilin A (CPA) was used as the reference gene in qPCR analysis. f,g) WB of BMAL1 protein (n = 4, 4) and qPCR analysis of Bmal1 gene expression (n = 6, 6) in the eWAT of WT and 2KR mice. Cyclophilin A (CPA) was used as the reference gene in qPCR analysis. h) BMAL1 protein in the aKQ primary adipocytes after treatment with cycloheximide (CHX) time course. Data are presented as mean ± SEM, *p < 0.05 and **p < 0.01 by two‐tailed Student's t‐test.