Fig. 4

TP deficiency alters adipocyte function of ASC. Data were obtained in ASC, ASC with a CRISPR-Cas9-mediated TP-knockout (KO), and ASC transduced with a Cas9/scramble gRNA plasmid corresponding to control (CTL) cells. A Protein expression of adipocyte markers obtained by Western blotting during in vitro adipocyte differentiation of ASC cells at D0 (undifferentiated state) and D20 (day 20 after differentiation onset). Numbers on the left correspond to molecular weight markers (kDa). Western blot images are representative of three independent experiments. PPARγ: peroxisome proliferator-activated receptor-gamma; C/EBPα: CCAAT/enhancer-binding protein-alpha; SREBP-1c: sterol regulatory element-binding protein-1c; FAS: fatty acid synthase. B Activation of insulin signaling in adipocytes after 20 days of adipocyte differentiation. ASC, CTL, and TP KO cells were deprived of serum for 6 h, stimulated with 20 nM insulin for 5 min or left untreated, and subjected to immunoblotting with antibodies against total and phospho-insulin receptor β-subunit (IRβ), insulin receptor substrate-1 (IRS1), AKT, and extracellular-regulated kinase (ERK)1/2. Numbers on the left correspond to molecular weight markers (kDa). Western blot images are representative of three independent experiments. C Activation of insulin signaling in ASC before differentiation at D0. Same as in B in undifferentiated ASC. Western blot images are representative of three independent experiments