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fasn  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc fasn
    METTL1-deficient MSCs inhibit lipid synthesis in hepatocytes. (A) Representative images of Nile Red staining in hepatocytes co-cultured with MSC shGFP and MSC shMETTL1 following treatment with FFA (Scale bar = 20 μm). (B) Measurement of TG content in hepatocytes in the indicated groups. (C, D) Western blot analysis of lipid metabolism-related gene expression <t>(FASN,</t> <t>SREBP1,</t> <t>SCD1)</t> in the indicated groups. (E, F) qPCR analysis of lipid synthesis gene expression ( Fasn, Scd1, Srebp1, Fads1 and Acaca ) in AML12 and HepG2 cells co-cultured with MSC shGFP and MSC shMETTL1 . For all statistical graphs, data are presented as mean ± S.E.M, with statistical significance is indicated in the figure.
    Fasn, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/fasn/pmc13032905-118-17-10
    Average 86 stars, based on 1 article reviews
    fasn - by Bioz Stars, 2026-10
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    Images

    1) Product Images from "METTL1-deficient mesenchymal stem cells protect against metabolic-associated fatty liver disease by increasing NAMPT secretion"

    Article Title: METTL1-deficient mesenchymal stem cells protect against metabolic-associated fatty liver disease by increasing NAMPT secretion

    Journal: Stem Cells Translational Medicine

    doi: 10.1093/stcltm/szag016

    METTL1-deficient MSCs inhibit lipid synthesis in hepatocytes. (A) Representative images of Nile Red staining in hepatocytes co-cultured with MSC shGFP and MSC shMETTL1 following treatment with FFA (Scale bar = 20 μm). (B) Measurement of TG content in hepatocytes in the indicated groups. (C, D) Western blot analysis of lipid metabolism-related gene expression (FASN, SREBP1, SCD1) in the indicated groups. (E, F) qPCR analysis of lipid synthesis gene expression ( Fasn, Scd1, Srebp1, Fads1 and Acaca ) in AML12 and HepG2 cells co-cultured with MSC shGFP and MSC shMETTL1 . For all statistical graphs, data are presented as mean ± S.E.M, with statistical significance is indicated in the figure.
    Figure Legend Snippet: METTL1-deficient MSCs inhibit lipid synthesis in hepatocytes. (A) Representative images of Nile Red staining in hepatocytes co-cultured with MSC shGFP and MSC shMETTL1 following treatment with FFA (Scale bar = 20 μm). (B) Measurement of TG content in hepatocytes in the indicated groups. (C, D) Western blot analysis of lipid metabolism-related gene expression (FASN, SREBP1, SCD1) in the indicated groups. (E, F) qPCR analysis of lipid synthesis gene expression ( Fasn, Scd1, Srebp1, Fads1 and Acaca ) in AML12 and HepG2 cells co-cultured with MSC shGFP and MSC shMETTL1 . For all statistical graphs, data are presented as mean ± S.E.M, with statistical significance is indicated in the figure.

    Techniques Used: Staining, Cell Culture, Western Blot, Gene Expression

    Transplantation of METTL1-deficient MSCs alleviates metabolic disorders associated with MASLD. (A) Schematic diagram of the animal experiment. (B) Evaluation of liver weight and the liver-to-body weight ratio in the indicated mice. (C) Assessment of fasting blood glucose levels in the indicated mice. (D) Analysis of GTT and ITT for the indicated groups. (E) Measurement of serum ALT and AST levels following 7 weeks of cell transplantation. (F) Representative images of HE and Oil Red O staining for analysis of mouse liver tissue (Scale bar = 100 μm). (G) Determination of TG and TC levels in the liver tissue of the specified mice. (H) qPCR analysis of lipid synthesis-related genes, including Fasn, Scd1, Srebp1, Fads1 , and Acaca in the specified groups. (I) Western blot analysis of lipid metabolism-related proteins in the specified groups. For all statistical graphs, individual data points represent individual mice, and data are presented as mean ± S.E.M. Statistical significance is indicated as shown in the figure.
    Figure Legend Snippet: Transplantation of METTL1-deficient MSCs alleviates metabolic disorders associated with MASLD. (A) Schematic diagram of the animal experiment. (B) Evaluation of liver weight and the liver-to-body weight ratio in the indicated mice. (C) Assessment of fasting blood glucose levels in the indicated mice. (D) Analysis of GTT and ITT for the indicated groups. (E) Measurement of serum ALT and AST levels following 7 weeks of cell transplantation. (F) Representative images of HE and Oil Red O staining for analysis of mouse liver tissue (Scale bar = 100 μm). (G) Determination of TG and TC levels in the liver tissue of the specified mice. (H) qPCR analysis of lipid synthesis-related genes, including Fasn, Scd1, Srebp1, Fads1 , and Acaca in the specified groups. (I) Western blot analysis of lipid metabolism-related proteins in the specified groups. For all statistical graphs, individual data points represent individual mice, and data are presented as mean ± S.E.M. Statistical significance is indicated as shown in the figure.

    Techniques Used: Transplantation Assay, Staining, Western Blot

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    Article Snippet: Next, membranes were incubated for 1 h at room temperature with the corresponding Horseradish peroxidase (HRP)-conjugated immunoglobulin G (IgG) secondary antibody (Mouse immunoglobulin G (IgG) (7074) (Cell Signaling Technologies, Danvers, MA, USA) at 1:2,000 (v/v) ratio dilution).

    Article Title: A novel arctigenin derivative attenuates nonalcoholic fatty liver disease by activating adiponectin receptor 1-mediated AMPK signaling pathway.
    Article Snippet: Nonalcoholic fatty liver disease (NAFLD), along with metabolic syndrome and obesity, has seen a dramatic rise in frequency around the world.. Arctigenin (ATG) has better efficacy in the treatment of non-alcoholic fatty liver in vitro, but its application in vivo models is limited due to its low oral bioavailability and poor water solubility.. Compound ARC-18 is a derivative of ATG.

    Western Blot:

    Article Title: Tofogliflozin attenuates liver steatosis and fibrosis in non-diabetic non-alcoholic steatohepatitis mice.
    Article Snippet: .. The primary antibodies used in immunoblotting included antibodies against acetyl-CoA carboxylase (ACC) (#3676, Cell Signaling Technology, MA, USA), cluster of differentiation 36 (CD36) (#28109, Cell Signaling Technology), carnitine palmitoyltransferase 1a (CPT1a) (ab234111, Abcam), fatty acid synthase (FASN) (#3180, Cell Signaling Technology), fatty acid transport protein 2 (FATP2) (#78771, Cell Signaling Technology), farnesoid X receptor (FXR) (#72105, Cell Signaling Technology), and sterol regulatory element binding protein1c (SREBP-1c) (sc-13551, Santa Cruz Biotechnology, TX, USA). .. The membranes were washed with TBST and incubated with goat anti-rabbit (#31460, Thermo Fisher Scientific, MA, USA) or goat anti-mouse secondary antibodies (#31430, Thermo Fisher Scientific) at room temperature for 1 h. The blots were incubated with β-actin (#4970, Cell Signaling Technology) as a loading control.

    Binding Assay:

    Article Title: Tofogliflozin attenuates liver steatosis and fibrosis in non-diabetic non-alcoholic steatohepatitis mice.
    Article Snippet: .. The primary antibodies used in immunoblotting included antibodies against acetyl-CoA carboxylase (ACC) (#3676, Cell Signaling Technology, MA, USA), cluster of differentiation 36 (CD36) (#28109, Cell Signaling Technology), carnitine palmitoyltransferase 1a (CPT1a) (ab234111, Abcam), fatty acid synthase (FASN) (#3180, Cell Signaling Technology), fatty acid transport protein 2 (FATP2) (#78771, Cell Signaling Technology), farnesoid X receptor (FXR) (#72105, Cell Signaling Technology), and sterol regulatory element binding protein1c (SREBP-1c) (sc-13551, Santa Cruz Biotechnology, TX, USA). .. The membranes were washed with TBST and incubated with goat anti-rabbit (#31460, Thermo Fisher Scientific, MA, USA) or goat anti-mouse secondary antibodies (#31430, Thermo Fisher Scientific) at room temperature for 1 h. The blots were incubated with β-actin (#4970, Cell Signaling Technology) as a loading control.



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    Figure Lengend Snippet: Pathway enrichment analysis of the 25-gene signature. (A) Reactome enrichment analysis identified significant pathways, including fatty acid metabolism, cholesterol biosynthesis, and nuclear receptor signaling. (B) WikiPathways analysis corroborated the involvement of these genes in lipid metabolism pathways, including SREBF and MIR33 (microRNA 33) in cholesterol and lipid homeostasis. (C) Gene–pathway interaction network highlighting the central roles of lipid metabolism regulators fatty acid (FA) synthase ( FASN ) and stearoyl-coenzyme A (CoA) desaturase ( SCD ) and other genes involved in the cell cycle and membrane trafficking, including TPD52 like 1 ( TPD52L1 ), leucine-rich repeats and immunoglobulin-like domains 1 ( LRIG1 ), keratin 7 ( KRT7 ), homeobox C4 ( HOXC4 ), and CDC42 effector protein 3 ( CDC42EP3 ).

    Article Snippet: In summary, 5,637 cells (1,000 cells per well) and J82 cells (500 cells per well) were seeded into 6-well plates and incubated at 37 °C for 24 h. The following day, one group served as the control and was maintained in the growth medium, while the experimental group received an addition of 50 μM FASN inhibitor (MedChemExpress, TVB-3664, catalog no. HY-120062) and SCD inhibitor (MedChemExpress, A939572, catalog no. HY-50709) to the growth medium and was cultured for a duration of 13 d. Subsequently, the cells were fixed with 4% formaldehyde (Sigma-Aldrich) and stained with 0.5% crystal violet (Sigma-Aldrich).

    Techniques: Membrane

    Prognostic validation and functional assessment of lipid metabolism regulators, fatty acid synthase ( FASN ) and stearoyl-coenzyme A desaturase ( SCD ). (A) Kaplan–Meier survival analysis indicating the prognostic significance of high expression levels of FASN (hazard ratio [HR] = 1.41) and SCD (HR = 1.8) in patients with bladder cancer (BLCA). (B) Expression analysis across stages revealed no significant variation (ANOVA, P = 0.3). (C) Colony formation assays demonstrating significantly reduced proliferation in BLCA cell lines (J82 and 5637) treated with the FASN inhibitor (FASNi; TVB-3664) and SCD inhibitor (SCDi; A939572). (D) Migration assays confirmed significantly impaired motility upon FASN and SCD inhibition, underscoring their roles in tumor aggressiveness. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

    Journal: Computational and Structural Biotechnology Journal

    Article Title: Epigenomics-Guided Multi-Omics Integration Uncovers a Lipid-Metabolic Signature with Translational Utility in Bladder Cancer

    doi: 10.34133/csbj.0139

    Figure Lengend Snippet: Prognostic validation and functional assessment of lipid metabolism regulators, fatty acid synthase ( FASN ) and stearoyl-coenzyme A desaturase ( SCD ). (A) Kaplan–Meier survival analysis indicating the prognostic significance of high expression levels of FASN (hazard ratio [HR] = 1.41) and SCD (HR = 1.8) in patients with bladder cancer (BLCA). (B) Expression analysis across stages revealed no significant variation (ANOVA, P = 0.3). (C) Colony formation assays demonstrating significantly reduced proliferation in BLCA cell lines (J82 and 5637) treated with the FASN inhibitor (FASNi; TVB-3664) and SCD inhibitor (SCDi; A939572). (D) Migration assays confirmed significantly impaired motility upon FASN and SCD inhibition, underscoring their roles in tumor aggressiveness. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

    Article Snippet: In summary, 5,637 cells (1,000 cells per well) and J82 cells (500 cells per well) were seeded into 6-well plates and incubated at 37 °C for 24 h. The following day, one group served as the control and was maintained in the growth medium, while the experimental group received an addition of 50 μM FASN inhibitor (MedChemExpress, TVB-3664, catalog no. HY-120062) and SCD inhibitor (MedChemExpress, A939572, catalog no. HY-50709) to the growth medium and was cultured for a duration of 13 d. Subsequently, the cells were fixed with 4% formaldehyde (Sigma-Aldrich) and stained with 0.5% crystal violet (Sigma-Aldrich).

    Techniques: Biomarker Discovery, Functional Assay, Expressing, Migration, Inhibition

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    Article Title: A pan-tissue multi-omics resource atlas of coordinated immune, metabolic, and fibrotic alterations in diet-induced MASH

    doi: 10.1016/j.isci.2026.117139

    Figure Lengend Snippet:

    Article Snippet: Fatty Acid Synthase (FASN) Rabbit mAb , ABclonal , Cat# A19050; RRID: AB_2100796.

    Techniques: Recombinant, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Activity Assay, Transcriptomics, Mass Spectrometry, Reverse Transcription Polymerase Chain Reaction, Software

    Therapeutic targeting of KAT2B-low RCC with a FASN inhibitor (A-B) Representative images of IHC staining of FASN in RCC cohort and statistical analysis. (C) Representative images of IHC staining for FASN and KAT2B in RCC tissues with high and low KAT2B expression. (D) Scatter plot of the relationship among KAT2B expression and FASN expression in advanced RCC tumors (n = 53). (E) The cell viability of ACHN and Caki-1 cells after treated with TVB-2640 (n = 4). (F) The cell viability of 786O and 769P cells after treated with TVB-2640 (n = 10). Proteins from three independent sites in RCC tissues were extracted to detect KAT2B expression. (H) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM). 15 organoids were randomly selected from each group for statistical analysis. (I) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM) (n = 15). (J) Representative images of two PDOs with different KAT2B expression after treatment with TVB-2640 (n = 10). (K) Representative images of PRO-1 staining of PDOs. (L-M) The cell viability of ACHN cells (L) and case 1 primary RCC cells (M) with KAT2B knockdown after treated with TVB-2640 (n = 4). (N-O) The picture (N) of xenograft using 786O cells with KAT2B knockdown after treated with TVB-2640, and tumor growth curve (n = 4). Data were analyzed by unpaired t test (B, H, I, J), one-way ANOVA (O) or two-way ANOVA (E, F, G, L, M).

    Journal: Journal of Advanced Research

    Article Title: Epigenetically silenced KAT2B suppresses de novo lipogenesis through destroying HDAC5/LSD1 complex assembly in renal cell carcinoma

    doi: 10.1016/j.jare.2025.08.007

    Figure Lengend Snippet: Therapeutic targeting of KAT2B-low RCC with a FASN inhibitor (A-B) Representative images of IHC staining of FASN in RCC cohort and statistical analysis. (C) Representative images of IHC staining for FASN and KAT2B in RCC tissues with high and low KAT2B expression. (D) Scatter plot of the relationship among KAT2B expression and FASN expression in advanced RCC tumors (n = 53). (E) The cell viability of ACHN and Caki-1 cells after treated with TVB-2640 (n = 4). (F) The cell viability of 786O and 769P cells after treated with TVB-2640 (n = 10). Proteins from three independent sites in RCC tissues were extracted to detect KAT2B expression. (H) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM). 15 organoids were randomly selected from each group for statistical analysis. (I) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM) (n = 15). (J) Representative images of two PDOs with different KAT2B expression after treatment with TVB-2640 (n = 10). (K) Representative images of PRO-1 staining of PDOs. (L-M) The cell viability of ACHN cells (L) and case 1 primary RCC cells (M) with KAT2B knockdown after treated with TVB-2640 (n = 4). (N-O) The picture (N) of xenograft using 786O cells with KAT2B knockdown after treated with TVB-2640, and tumor growth curve (n = 4). Data were analyzed by unpaired t test (B, H, I, J), one-way ANOVA (O) or two-way ANOVA (E, F, G, L, M).

    Article Snippet: Four days after inoculation, the mice were randomly divided into two groups and treated with either the vehicle (30 % PEG400) or the FASN inhibitor TVB-2640 (HY-112829, MCE, USA) (100 mg/kg) once daily by oral gavage for 3 consecutive weeks.

    Techniques: Immunohistochemistry, Expressing, Staining, Knockdown