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. Author manuscript; available in PMC: 2024 Mar 20.
Published in final edited form as: Nat Metab. 2024 Jan 8;6(1):78–93. doi: 10.1038/s42255-023-00945-1

Extended Data Fig. 1 |. The mRNA levels of JunB were upregulated by inhibition of mTORC1 and by obesity in BAT, related to Fig. 1.

Extended Data Fig. 1 |

a. The layout of fold changes (rapamycin: control) of 96 genes that are cAMP responsive in PCR array analysis. The reverse transcription was performed with total RNA extracted from BAT in mice treated with or without rapamycin (n = 3/group), and then the synthesized cDNAs was used for PCR array analysis. b. RNA-sequencing gene expression signatures of iWAT from 10-week-old male Raptor KO and control mice. n = 2–3/group. c. The protein levels of JunB were upregulated by HFD feeding in adipose tissue. d. Quantification of JunB expression in Extended Data Figure c. e. mRNA levels of JunB were induced in WAT of HFD-fed mice (6 mice/group). f. mRNA levels of Ucp1 and Pgc-1α in human deep neck fat were negatively correlated with BMI. g. The expression pattern of JunB in adipocyte subsets and APCs in human BAT. h. Quantification the protein level in Fig. 1k. i. JunB is expressed in Plin1-enriched primary differentiated adipocytes. j. JunB was highly enriched in primary preadipocytes which declined during differentiation (n = 3, independent experiments). Statistical analysis was performed using Pearson’s correlation coefficient in Extended Data Fig. 1f. Extended Data Fig. 1d, e, h, j were analyzed using unpaired two-sided T-Test.