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Fig. 6 | Cell & Bioscience

Fig. 6

From: WRN loss accelerates abnormal adipocyte metabolism in Werner syndrome

Fig. 6

Hyperactive SMARCA5 causes the adipocyte prematurity in WS. a, b qRT-PCR analysis of SMARCA5 expression on days 1 (a) and 5 (b) among WT, WRN KO, and WRN overexpression adipocytes (WRN KO (WRN)) (N = 3 biological replicates). b qRT-PCR analysis of smarca5 expression at 2 dpf, 4 dpf, and 14 dpf among wildtype, wrn−/− mutant zebrafish, and wrn overexpression zebrafish (wrn−/− (WRN)) (N = 3 biological replicates). d–g qRT-PCR analysis of PPARγ, CEBPα, UCP1, and FABP4 on day 5 among WT, WRN KO, and WRN overexpression or SMARCA5 knock-down adipocytes. (N = 3 biological replicates). h, i qRT-PCR analysis of PER1 and RORB on day 5 among WT, WRN KO, and WRN overexpression or SMARCA5 knock-down adipocytes. (N = 3 biological replicates). j, k qRT-PCR analysis of pparγ and cebpα at 2 dpf, 4 dpf, and 14 dpf between wrn−/− mutant zebrafish and ASOs treated zebrafish (N = 3 biological replicates). l, m qRT-PCR analysis of per1a and rorb at 2 dpf, 4 dpf, and 14 dpf between wrn−/− mutant zebrafish and ASOs treated zebrafish (N = 3 biological replicates). n Illustration of three different regions in human SMARCA5 promoters selected for dual-luciferase assay. o Dual-luciferase assay analysis of SMARCA5 transcription activity (N = 3 biological replicates). Data are presented as the mean ± S.D. Statistical analysis was performed using two-tailed unpaired Student’s t-test. *P < 0.05, **P < 0.01, ***P < 0.001

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