CHREBP Antibody (2D9NB) - BSA Free NBP2-44307 from Novus Biologicals, a Bio-Techne Brand

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G3 (Bethesda, Md.)
July 09 2019

Fig 1: pLPD-induced down-regulation of lipogenic genes in F1 offspring iWAT. (A) Differential mRNA expression of selected lipogenic genes shown in Figure 1A was corroborated using qRT-PCR (n = 3). Gene expression was normalized to the reference gene 36B4, and actin was used as a negative control. Bars represent the mean ± SD *, P < 0.05; **, P < 0.01; ns, not significant; CD, control diet; LPD, low-protein diet. (B and C) The down-regulation of Pfkl and Ppp2r5b, and up-regulation of Igfbp2, in F1 iWAT was confirmed by qRT-PCR. (D) pLPD reduced the amount of ChREBP bound to the ChREBP-β gene promoter in F1 offspring iWAT, demonstrated using qChIP of F1 offspring iWAT and an anti-ChREBP antibody. Primers that amplified the region containing the ChREBP-β gene promoter were used for qPCR. Mean values relative to the input ± SD are shown (n = 3). *, P < 0.05; **, P < 0.01; ns, not significant. (E) A speculative scheme for the down-regulation of the lipogenic genes in F1 iWAT.
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Molecular metabolism
October 01 2022

Fig 2: CCNC deficiency inhibits the C/EBPα-GLUT4-ChREBP pathway in BAT. (A) qRT-PCR analysis of indicated genes expression in BAT from control and CcncUcp1(KO) mice. (B) qRT-PCR analysis of lipogenic genes expression in BAT from control and CcncMyf5(KO) mice. (C) Western blots analysis of FAS (fatty acid synthase), ACC1 (acetyl-CoA carboxylase-1), Nuclear form of SREBP1 and GLUT4 protein expression in BAT from control and CcncUcp1(KO) mice. (D) Dual-luciferase assays of Glut4 promoter (−469 bp) activity in WT and CCNC–KO brown preadipocytes transfected with GFP or C/EBPα. CRE, C/EBPα responsive-element. qRT-PCR analysis of Chrebp (E) and its target genes (F) expression in BAT from control and CcncUcp1(KO) mice. (G) qRT-PCR analysis of indicated genes expression in BAT from control and CcncMyf5(KO) mice. (H) Western blots analysis of CCNC and overexpressed ChREBPβ in WT and CCNC–KO brown preadipocytes. Overexpressed GFP was used as a transfection control. (I) Representative light pictures of differentiated WT and CCNC–KO brown adipocytes with overexpressed GFP or ChREBPβ. Scale bar, 50 μm. (J) qRT-PCR analysis of lipogenic genes expression in differentiated WT and CCNC–KO brown adipocytes with overexpressed GFP or ChREBPβ. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs control. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
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Molecular metabolism
October 01 2022

Fig 3: A model depicting the role of CCNC in BAT development and function. At embryonic stage (A), CCNC deletion in brown adipocyte progenitor cells results in prenatal BAT paucity due to impairment of brown adipocyte progenitor cell proliferation, while at postnatal stage (B), CCNC deficiency in mature brown adipocytes leads to reduced lipid accumulation because of the inhibition of C/EBPα-GLUT4-ChREBP -mediated lipid synthesis pathway. Thus, CCNC plays an important role in both BAT development and lipid accumulation in brown adipocytes. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)