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phosphorylated acetyl coa carboxylase p acc  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated acetyl coa carboxylase p acc
    Phosphorylated Acetyl Coa Carboxylase P Acc, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 2324 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/phosphorylated+p+acc/Acetyl-CoA+Carboxylase+Antibody/pm41861854-53-3-12
    Average 96 stars, based on 2324 article reviews
    phosphorylated acetyl coa carboxylase p acc - by Bioz Stars, 2026-09
    96/100 stars

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    other:

    Article Title: Accumulation of cholesterol, triglycerides and ceramides in hepatocellular carcinomas of diethylnitrosamine injected mice
    Article Snippet: Antibodies for glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (order number: 2118), phosphorylated (p)ACC (order number: 3661), pAMP-activated protein kinase (AMPK; order number: 2351), AMPK (order number: 2532), hormone sensitive lipase (HSL) (order number: 4107), stearoyl-CoA-reductase (SCD1) (order number: 2794), cyclophilin A (order number: 2175) and fatty acid synthase (FAS) (order number: 3189) were from Cell Signaling (Frankfurt am Main, Germany).

    Article Title: Polysaccharides from Armillariella tabescens mycelia ameliorate insulin resistance in type 2 diabetic mice.
    Article Snippet: Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by hyperglycemia mainly due to insulin resistance.. The objective of this study was to investigate the effects of polysaccharides from Armillariella tabescens mycelia (AT) on insulin resistance in mice fed a high-fat diet in combination with streptozotocin to induce T2DM.. Following treatment with different doses of AT, hyperglycemia and lipid metabolism dysfunction, insulin resistance, and hepatic function-related indices were markedly ameliorated; the histopathological alterations, oxidative stress, and inflammatory reaction in hepatic tissue were also alleviated; most importantly, AT inhibited the expression of hepatic thioredoxin-interacting protein (TXNIP) to repress the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome activation and activated the 5’AMP-activated protein kinase (AMPK) pathway in a dose-dependent manner in T2DM mice.

    Western Blot:

    Article Title: Postbiotic Metabolites of Proanthocyanidins Reduce Adipogenesis In Vitro by Suppressing De Novo Lipogenesis
    Article Snippet: CellTiter 96 ® aqueous MTS reagent powder (G1111) was purchased from Promega Corporation, Madison, WI, USA. .. The antibodies of the Western blotting technique, acetyl-CoA carboxylase (ACC, 3676S), phosphorylated ( p )-ACC (11818S), anti-mouse secondary antibody (7076P2), anti-rabbit secondary antibody (7074S), fatty acid synthase (FAS, 3180S), peroxisome proliferator-activated receptor- γ (PPAR- γ , 2443S), and β -actin (12620S) were purchased from Cell Signaling Technology, Inc., Danvers, MA, USA. ..

    Article Title: Postbiotic Metabolites of Proanthocyanidins Reduce Adipogenesis In Vitro by Suppressing De Novo Lipogenesis.
    Article Snippet: CellTiter 96® aqueous MTS reagent powder (G1111) was purchased from Promega Corporation, Madison, WI, USA. .. The antibodies of the Western blotting technique, acetyl-CoA carboxylase (ACC, 3676S), phosphorylated (p)-ACC (11818S), anti-mouse secondary antibody (7076P2), anti-rabbit secondary antibody (7074S), fatty acid synthase (FAS, 3180S), peroxisome proliferator-activated receptor-γ (PPAR-γ, 2443S), and β-actin (12620S) were purchased from Cell Signaling Technology, Inc., Danvers, MA, USA. ..

    Article Title: 4-1BBL signaling promotes cell proliferation through reprogramming of glucose metabolism in monocytes/macrophages.
    Article Snippet: Obesity-induced monocyte/macrophage proliferation and activation plays a crucial role in various chronic inflammatory metabolic disorders such as insulin resistance, diabetes mellitus, and atherosclerosis.. 4-1BBL, a member of the tumor necrosis factor superfamily expressed on monocytes/macrophages, provides inflammatory signals to modulate their proliferation, survival, and cytokine release.. Previously, we demonstrated that 4-1BBL signal promotes adipose inflammation through enhancement of macrophage activation.

    Saline:

    Article Title: Lipoatrophy-Associated Insulin Resistance and Hepatic Steatosis are Attenuated by Intake of Diet Rich in Omega 3 Fatty Acids.
    Article Snippet: 195 words) Scope: We evaluated glucose homeostasis and progression of nonalcoholic fatty liver disease (NAFLD) and hepatomegaly in severe lipoatrophic mice and their modulation by intake of a diet rich in omega 3 (n-3) fatty acids (HFO).. Methods and results: Severe lipoatrophic mice induced by PPARγ deletion exclusively in adipocytes (A-PPARγ KO) and littermate controls (A-PPARγ WT) were evaluated for glucose homeostasis and liver mass, proteomics, lipidomics, inflammation and fibrosis.. Lipoatrophic mice were heavier than controls, severely glucose intolerant and hyperinsulinemic, and developed NAFLD characterized by increased liver glycogen, triacylglycerol and diacylglycerol contents, mitotic index, apoptosis, inflammation, steatosis score, fibrosis and fatty acid synthase (FAS) content and activity.



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    phosphorylated acetyl coa carboxylase p acc  (Cell Signaling Technology Inc)
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    phosphorylated acc p acc  (Cell Signaling Technology Inc)
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    Fig. 4. Effects of KFS on the hepatic <t>AMPK–ACC</t> axis in mice fed a MCD diet for 6 weeks. Hepatic AMPKα (A, B) and ACC (C, D) levels were assessed via immunoblot analysis of liver homogenates. (A, C) AMPKα, <t>phosphorylated</t> AMPKα (p-AMPKα), ACC and phosphorylated <t>ACC</t> <t>(p-ACC)</t> levels were assessed in liver homogenates prepared from the mice in each group. Gapdh was used as the loading control. (B, D) The graphs show the ratios of the phosphorylated forms of AMPKα and ACC. The data are presented as levels relative to those in the chow-fed group. Mean ± SD (n = 3). MCD, MCD diet group; MCD + KFS, MCD diet with KFS administration group. *** p < 0.001 and ** p < 0.01, and * p < 0.05 vs. MCD by Dunnett’s test.
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    anti-phosphorylated acetyl-coa carboxylase (p-acc)  (Cell Signaling Technology Inc)
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    Fig. 4. Effects of KFS on the hepatic <t>AMPK–ACC</t> axis in mice fed a MCD diet for 6 weeks. Hepatic AMPKα (A, B) and ACC (C, D) levels were assessed via immunoblot analysis of liver homogenates. (A, C) AMPKα, <t>phosphorylated</t> AMPKα (p-AMPKα), ACC and phosphorylated <t>ACC</t> <t>(p-ACC)</t> levels were assessed in liver homogenates prepared from the mice in each group. Gapdh was used as the loading control. (B, D) The graphs show the ratios of the phosphorylated forms of AMPKα and ACC. The data are presented as levels relative to those in the chow-fed group. Mean ± SD (n = 3). MCD, MCD diet group; MCD + KFS, MCD diet with KFS administration group. *** p < 0.001 and ** p < 0.01, and * p < 0.05 vs. MCD by Dunnett’s test.
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    Fig. 5. Effects of HDCA on the relative expressions of lipid metabolism-related factors in 3T3-L1 mature adipocytes. (A-B) Effects of HDCA on the levels of lipid metabolism-related gene expression; n ¼ 6. (C-D) Relative protein expressions and grayscale analysis of lipid metabolism-related factors in HDCA-treated groups; n ¼ 3. Values with different letters mean significant difference (P < 0.05). <t>ACC</t> ¼ acetyl-CoA-carboxylase; C/EBPa ¼ enhancer binding proteins alpha; FXR ¼ farnesoid X receptor; TGR5 ¼ Takeda G-protein-coupled receptor 5; SREBP-1c ¼ sterol regulatory element-binding protein-1c; FABP4 ¼ fatty acid binding protein 4; PPARG ¼ peroxisome proliferator-activated receptor gamma; HSL ¼ hormone-sensitive triglyceride lipase; p-HSL ¼ <t>phosphorylated</t> hormone-sensitive triglyceride <t>lipase;</t> <t>p-ACC</t> ¼ phosphorylated acetyl-CoA-carboxylase; HDCA ¼ hyodeoxycholic acid; GW4064 ¼ the farnesoid X receptor agonist.
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    Fig. 4. Effects of KFS on the hepatic AMPK–ACC axis in mice fed a MCD diet for 6 weeks. Hepatic AMPKα (A, B) and ACC (C, D) levels were assessed via immunoblot analysis of liver homogenates. (A, C) AMPKα, phosphorylated AMPKα (p-AMPKα), ACC and phosphorylated ACC (p-ACC) levels were assessed in liver homogenates prepared from the mice in each group. Gapdh was used as the loading control. (B, D) The graphs show the ratios of the phosphorylated forms of AMPKα and ACC. The data are presented as levels relative to those in the chow-fed group. Mean ± SD (n = 3). MCD, MCD diet group; MCD + KFS, MCD diet with KFS administration group. *** p < 0.001 and ** p < 0.01, and * p < 0.05 vs. MCD by Dunnett’s test.

    Journal: Journal of Functional Foods

    Article Title: Alleviating effects of koji-fermented soybean extract on nonalcoholic steatohepatitis in mice through inactivation of acetyl-CoA carboxylase without inhibition of AMPK

    doi: 10.1016/j.jff.2025.106927

    Figure Lengend Snippet: Fig. 4. Effects of KFS on the hepatic AMPK–ACC axis in mice fed a MCD diet for 6 weeks. Hepatic AMPKα (A, B) and ACC (C, D) levels were assessed via immunoblot analysis of liver homogenates. (A, C) AMPKα, phosphorylated AMPKα (p-AMPKα), ACC and phosphorylated ACC (p-ACC) levels were assessed in liver homogenates prepared from the mice in each group. Gapdh was used as the loading control. (B, D) The graphs show the ratios of the phosphorylated forms of AMPKα and ACC. The data are presented as levels relative to those in the chow-fed group. Mean ± SD (n = 3). MCD, MCD diet group; MCD + KFS, MCD diet with KFS administration group. *** p < 0.001 and ** p < 0.01, and * p < 0.05 vs. MCD by Dunnett’s test.

    Article Snippet: We used antibodies against AMP kinase α (AMPKα), phosphorylated AMPK (pAMPK), acetyl-CoA carboxylase (ACC) and phosphorylated ACC (p-ACC) (Cell Signaling Technology, Danvers, MA) (Table S3).

    Techniques: Western Blot, Control

    Fig. 5. Effects of HDCA on the relative expressions of lipid metabolism-related factors in 3T3-L1 mature adipocytes. (A-B) Effects of HDCA on the levels of lipid metabolism-related gene expression; n ¼ 6. (C-D) Relative protein expressions and grayscale analysis of lipid metabolism-related factors in HDCA-treated groups; n ¼ 3. Values with different letters mean significant difference (P < 0.05). ACC ¼ acetyl-CoA-carboxylase; C/EBPa ¼ enhancer binding proteins alpha; FXR ¼ farnesoid X receptor; TGR5 ¼ Takeda G-protein-coupled receptor 5; SREBP-1c ¼ sterol regulatory element-binding protein-1c; FABP4 ¼ fatty acid binding protein 4; PPARG ¼ peroxisome proliferator-activated receptor gamma; HSL ¼ hormone-sensitive triglyceride lipase; p-HSL ¼ phosphorylated hormone-sensitive triglyceride lipase; p-ACC ¼ phosphorylated acetyl-CoA-carboxylase; HDCA ¼ hyodeoxycholic acid; GW4064 ¼ the farnesoid X receptor agonist.

    Journal: Animal Nutrition

    Article Title: Different types of bile acids exhibit opposite regulatory effects on lipid metabolism in finishing pigs through bile acid receptors

    doi: 10.1016/j.aninu.2024.12.003

    Figure Lengend Snippet: Fig. 5. Effects of HDCA on the relative expressions of lipid metabolism-related factors in 3T3-L1 mature adipocytes. (A-B) Effects of HDCA on the levels of lipid metabolism-related gene expression; n ¼ 6. (C-D) Relative protein expressions and grayscale analysis of lipid metabolism-related factors in HDCA-treated groups; n ¼ 3. Values with different letters mean significant difference (P < 0.05). ACC ¼ acetyl-CoA-carboxylase; C/EBPa ¼ enhancer binding proteins alpha; FXR ¼ farnesoid X receptor; TGR5 ¼ Takeda G-protein-coupled receptor 5; SREBP-1c ¼ sterol regulatory element-binding protein-1c; FABP4 ¼ fatty acid binding protein 4; PPARG ¼ peroxisome proliferator-activated receptor gamma; HSL ¼ hormone-sensitive triglyceride lipase; p-HSL ¼ phosphorylated hormone-sensitive triglyceride lipase; p-ACC ¼ phosphorylated acetyl-CoA-carboxylase; HDCA ¼ hyodeoxycholic acid; GW4064 ¼ the farnesoid X receptor agonist.

    Article Snippet: The primary antibodies against HSL (4107, Cell Signaling Technology, Danvers, MA, USA), p-HSL (45804, Cell Signaling Technology, Danvers, MA, USA), phosphorylated acetyl-CoAcarboxylase (p-ACC) (42801, Cell Signaling Technology, Danvers, MA, USA), Takeda G-protein-coupled receptor 5 (TGR5) (ab72608, Abcam, UK), peroxisome proliferator activated receptor gamma (PPARG) (2443, Cell Signaling Technology, Danvers, MA, USA), bactin (4967, Cell Signaling Technology, Danvers, MA, USA) and GAPDH (97166, Cell Signaling Technology, Danvers, MA, USA) were diluted to a concentration of 1:1000.

    Techniques: Gene Expression, Binding Assay