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rabbit polyclonal phospho acetyl coa carboxylase p acc  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit polyclonal phospho acetyl coa carboxylase p acc
    Nic plus Coke administration increases the lipogenesis marker in the liver. (A) Representative western blot analysis of SREBP1 cleavage (SREBP1c). β-Actin levels are shown as a loading control. Molecular weight markers are depicted in KDa. (B) Quantification of the western blot of SREBP1c. (C) Representative western blot analysis <t>of</t> <t>p-ACC.</t> β-Actin levels are shown as a loading control. Molecular weight markers are depicted in KDa. (D) Quantification of the western blot of p-ACC. Protein levels of SREBP1c and p-ACC were normalized to β-Actin and expressed as the mean ± S.E.M. (the fold of change relative to the control). n= 5 - 6 per group. Statistical difference is indicated by * compared to Sal+Water vs Nic+Coke (P< 0.05).
    Rabbit Polyclonal Phospho Acetyl Coa Carboxylase P Acc, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 3027 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+polyclonal+anti+p+acc+ser79/Phospho-Acetyl-CoA+Carboxylase+(Ser79)+Antibody/pmc11097688-70-15-22
    Average 96 stars, based on 3027 article reviews
    rabbit polyclonal phospho acetyl coa carboxylase p acc - by Bioz Stars, 2026-09
    96/100 stars

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    1) Product Images from "Hepatic steatosis induced by nicotine plus Coca-Cola™ is prevented by nicotinamide riboside (NR)"

    Article Title: Hepatic steatosis induced by nicotine plus Coca-Cola™ is prevented by nicotinamide riboside (NR)

    Journal: Frontiers in Endocrinology

    doi: 10.3389/fendo.2024.1282231

    Nic plus Coke administration increases the lipogenesis marker in the liver. (A) Representative western blot analysis of SREBP1 cleavage (SREBP1c). β-Actin levels are shown as a loading control. Molecular weight markers are depicted in KDa. (B) Quantification of the western blot of SREBP1c. (C) Representative western blot analysis of p-ACC. β-Actin levels are shown as a loading control. Molecular weight markers are depicted in KDa. (D) Quantification of the western blot of p-ACC. Protein levels of SREBP1c and p-ACC were normalized to β-Actin and expressed as the mean ± S.E.M. (the fold of change relative to the control). n= 5 - 6 per group. Statistical difference is indicated by * compared to Sal+Water vs Nic+Coke (P< 0.05).
    Figure Legend Snippet: Nic plus Coke administration increases the lipogenesis marker in the liver. (A) Representative western blot analysis of SREBP1 cleavage (SREBP1c). β-Actin levels are shown as a loading control. Molecular weight markers are depicted in KDa. (B) Quantification of the western blot of SREBP1c. (C) Representative western blot analysis of p-ACC. β-Actin levels are shown as a loading control. Molecular weight markers are depicted in KDa. (D) Quantification of the western blot of p-ACC. Protein levels of SREBP1c and p-ACC were normalized to β-Actin and expressed as the mean ± S.E.M. (the fold of change relative to the control). n= 5 - 6 per group. Statistical difference is indicated by * compared to Sal+Water vs Nic+Coke (P< 0.05).

    Techniques Used: Marker, Western Blot, Control, Molecular Weight

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    Article Snippet: 26 Metformin, an adenosine monophosphate-activated protein kinase (AMPK) 27 activator, has been shown in previous studies to reduce kidney fibrosis in different 28 models of experimental chronic kidney disease (CKD).. However, in all of these studies, 29 the administration of metformin was initiated before the establishment of renal disease, 30 which is a condition that does not typically occur in clinical settings.. The aim of the 31 present study was to investigate whether the administration of metformin could arrest 32 the progression of established renal disease in a well-recognized model of CKD, the 33 subtotal kidney nephrectomy (Nx) model.

    Incubation:

    Article Title: Metformin arrests the progression of established kidney disease in the subtotal nephrectomy model of chronic kidney disease.
    Article Snippet: 26 Metformin, an adenosine monophosphate-activated protein kinase (AMPK) 27 activator, has been shown in previous studies to reduce kidney fibrosis in different 28 models of experimental chronic kidney disease (CKD).. However, in all of these studies, 29 the administration of metformin was initiated before the establishment of renal disease, 30 which is a condition that does not typically occur in clinical settings.. The aim of the 31 present study was to investigate whether the administration of metformin could arrest 32 the progression of established renal disease in a well-recognized model of CKD, the 33 subtotal kidney nephrectomy (Nx) model.



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    Nic plus Coke administration increases the lipogenesis marker in the liver. (A) Representative western blot analysis of SREBP1 cleavage (SREBP1c). β-Actin levels are shown as a loading control. Molecular weight markers are depicted in KDa. (B) Quantification of the western blot of SREBP1c. (C) Representative western blot analysis <t>of</t> <t>p-ACC.</t> β-Actin levels are shown as a loading control. Molecular weight markers are depicted in KDa. (D) Quantification of the western blot of p-ACC. Protein levels of SREBP1c and p-ACC were normalized to β-Actin and expressed as the mean ± S.E.M. (the fold of change relative to the control). n= 5 - 6 per group. Statistical difference is indicated by * compared to Sal+Water vs Nic+Coke (P< 0.05).
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    Image Search Results


    Nic plus Coke administration increases the lipogenesis marker in the liver. (A) Representative western blot analysis of SREBP1 cleavage (SREBP1c). β-Actin levels are shown as a loading control. Molecular weight markers are depicted in KDa. (B) Quantification of the western blot of SREBP1c. (C) Representative western blot analysis of p-ACC. β-Actin levels are shown as a loading control. Molecular weight markers are depicted in KDa. (D) Quantification of the western blot of p-ACC. Protein levels of SREBP1c and p-ACC were normalized to β-Actin and expressed as the mean ± S.E.M. (the fold of change relative to the control). n= 5 - 6 per group. Statistical difference is indicated by * compared to Sal+Water vs Nic+Coke (P< 0.05).

    Journal: Frontiers in Endocrinology

    Article Title: Hepatic steatosis induced by nicotine plus Coca-Cola™ is prevented by nicotinamide riboside (NR)

    doi: 10.3389/fendo.2024.1282231

    Figure Lengend Snippet: Nic plus Coke administration increases the lipogenesis marker in the liver. (A) Representative western blot analysis of SREBP1 cleavage (SREBP1c). β-Actin levels are shown as a loading control. Molecular weight markers are depicted in KDa. (B) Quantification of the western blot of SREBP1c. (C) Representative western blot analysis of p-ACC. β-Actin levels are shown as a loading control. Molecular weight markers are depicted in KDa. (D) Quantification of the western blot of p-ACC. Protein levels of SREBP1c and p-ACC were normalized to β-Actin and expressed as the mean ± S.E.M. (the fold of change relative to the control). n= 5 - 6 per group. Statistical difference is indicated by * compared to Sal+Water vs Nic+Coke (P< 0.05).

    Article Snippet: We then incubated the membranes with the following first antibodies (diluted in blocking solution) including, rabbit polyclonal phospho-Acetyl-CoA Carboxylase (p-ACC) (1:1000) (3661; Cell Signaling Technology, Beverly, MA, USA), rabbit polyclonal phospho-AMP-activated protein kinase (p-AMPK) (1:1000) (2535; Cell Signaling Technology, Beverly, MA, USA), rabbit polyclonal HO-1 (1:2000) (AB13243; Abcam, San Francisco, CA, USA), mouse monoclonal Mitochondrial complex cocktail (1:3000) (AB110413; Abcam, San Francisco, CA, USA), rabbit polyclonal NAMPT (1:250) (AB45890; Abcam, San Francisco, CA, USA), rabbit polyclonal PGC1 α (1:1000) (AB54481; Abcam, San Francisco, CA, USA), rabbit polyclonal Sirt1 (1:2000) (AB12193; Abcam, San Francisco, CA, USA), rabbit polyclonal SOD2 (1:500) (sc-30080; Santa Cruz Biotechnology, Santa Cruz, CA, USA), mouse monoclonal SREBP1 (1:500) (AB3259; Abcam, San Francisco, CA, USA), and rabbit polyclonal β -Actin (1:4000) (AB8227; Abcam, San Francisco, CA, USA). β -Actin was used as a loading control, all antibodies were incubated overnight at 4°C with constant shaking.

    Techniques: Marker, Western Blot, Control, Molecular Weight