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anti scd1  (Cell Signaling Technology Inc)


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  • 95

    Structured Review

    Cell Signaling Technology Inc anti scd1
    Anti Scd1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 224 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/scd1/SCD1+Rabbit+mAb/pm41935215-265-21-22
    Average 95 stars, based on 224 article reviews
    anti scd1 - by Bioz Stars, 2026-09
    95/100 stars

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    Related Articles

    Staining:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Cell Culture:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Western Blot:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Gene Expression:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Transplantation Assay:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Expressing:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Inhibition:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    In Vitro:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Control:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Colorimetric Assay:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Flow Cytometry:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Injection:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Immunohistochemical staining:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Methylation:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Modification:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Quantitative RT-PCR:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Marker:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Luciferase:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Membrane:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Transmission Assay:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Electron Microscopy:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Over Expression:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).

    Immunohistochemistry:

    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.

    Article Title: RNF186 controls glucose metabolism in metabolic dysfunction-associated fatty liver disease.
    Article Snippet: Primary antibodies specific for the following proteins were purchased from Cell Signaling Technology: AKT (#4691), p-AKT (Ser473) (#4060), p-GSK3β (#9322), GSK3β (#12456), Fasn (#3180), GCK (#3782), SCD1 (#2794), IRS-1 (#2382), p-IRS-1 (#2388), PI3K (#4292), p-PI3K (#4288), FoxO1 (#2880), p-FoxO1 (#9461), JNK (#9252), p-JNK (#4668), GS (#3886), Ubiqutin (#3936), and HKII (#2867), p-eIF2α (#3398), eIF2α (#9722).



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    MedChemExpress scd1 expression
    PSM upregulates hepatic <t>SCD1</t> by enriching L. johnsonii . (a) Relative gene expression of hepatic SCD1 ( n =6). (b) Hepatic protein level of SCD1 was assessed by Western blotting and the densitometric quantification ( n =3). (c) Schematic diagram of the mouse experiment. (d) Relative expression of hepatic SCD1 and its upstream regulatory genes ( n =6). (e) Protein level of hepatic SCD1 in the CTRL, PSM alone and ABX+PSM groups, along with densitometric quantification ( n =3). (f) Relative abundance of altered microbiota by PSM alone at the genus level ( n =6). (g) Relative abundance of three Lactobacillus species in stool samples quantified by QPCR ( n =5). (h) Differential abundance of the fecal microbiota at the species level ( n =6). (i) Relative abundance of L. johnsonii was increased in the PSM alone group ( n =6). (j) Relative abundance of L. johnsonii in each group ( n =6). (k) Correlation analysis of the relative abundance of L. johnsonii and hepatic SCD1 protein expression. (l) Growth curves of L. johnsonii cultured with different concentrations of PSM at the indicated time points ( n =3). (m) Bacterial colony counts of L. johnsonii . *, # p < 0.05, *, ## p < 0.01, *, ### p < 0.001.
    Scd1 Expression, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Protein expression levels ( A , H ) including ( B ) PPARγ, ( C ) Fabp4, ( D ) CD36, ( E ) SREBP-1c, ( F ) ADIPOQ, ( G ) <t>SCD-1,</t> ( I ) TLR4, ( J ) IKKβ, and ( K ) p-P65 in liver tissues among NCD, HFCD, and HFCD + HB-1. Data were expressed as mean ± SD ( n = 3) based on Dunnett’s test. ** indicated p < 0.01, *** indicated p < 0.001, **** indicated p < 0.0001.
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    Image Search Results


    PSM upregulates hepatic SCD1 by enriching L. johnsonii . (a) Relative gene expression of hepatic SCD1 ( n =6). (b) Hepatic protein level of SCD1 was assessed by Western blotting and the densitometric quantification ( n =3). (c) Schematic diagram of the mouse experiment. (d) Relative expression of hepatic SCD1 and its upstream regulatory genes ( n =6). (e) Protein level of hepatic SCD1 in the CTRL, PSM alone and ABX+PSM groups, along with densitometric quantification ( n =3). (f) Relative abundance of altered microbiota by PSM alone at the genus level ( n =6). (g) Relative abundance of three Lactobacillus species in stool samples quantified by QPCR ( n =5). (h) Differential abundance of the fecal microbiota at the species level ( n =6). (i) Relative abundance of L. johnsonii was increased in the PSM alone group ( n =6). (j) Relative abundance of L. johnsonii in each group ( n =6). (k) Correlation analysis of the relative abundance of L. johnsonii and hepatic SCD1 protein expression. (l) Growth curves of L. johnsonii cultured with different concentrations of PSM at the indicated time points ( n =3). (m) Bacterial colony counts of L. johnsonii . *, # p < 0.05, *, ## p < 0.01, *, ### p < 0.001.

    Journal: Gut Microbes

    Article Title: Lactobacillus johnsonii mediates the protective effects of pristimerin against ulcerative colitis and concomitant liver injury through remodeling hepatic lipid metabolism via LXRα–SCD1 axis

    doi: 10.1080/19490976.2026.2701349

    Figure Lengend Snippet: PSM upregulates hepatic SCD1 by enriching L. johnsonii . (a) Relative gene expression of hepatic SCD1 ( n =6). (b) Hepatic protein level of SCD1 was assessed by Western blotting and the densitometric quantification ( n =3). (c) Schematic diagram of the mouse experiment. (d) Relative expression of hepatic SCD1 and its upstream regulatory genes ( n =6). (e) Protein level of hepatic SCD1 in the CTRL, PSM alone and ABX+PSM groups, along with densitometric quantification ( n =3). (f) Relative abundance of altered microbiota by PSM alone at the genus level ( n =6). (g) Relative abundance of three Lactobacillus species in stool samples quantified by QPCR ( n =5). (h) Differential abundance of the fecal microbiota at the species level ( n =6). (i) Relative abundance of L. johnsonii was increased in the PSM alone group ( n =6). (j) Relative abundance of L. johnsonii in each group ( n =6). (k) Correlation analysis of the relative abundance of L. johnsonii and hepatic SCD1 protein expression. (l) Growth curves of L. johnsonii cultured with different concentrations of PSM at the indicated time points ( n =3). (m) Bacterial colony counts of L. johnsonii . *, # p < 0.05, *, ## p < 0.01, *, ### p < 0.001.

    Article Snippet: Animal experiment 6 : PPARα KO-induced increase in hepatic SCD1 expression protected against colitis study, male 129/Sv wild-type mice (WT) were randomly classified into three groups ( n =5): (1) WT-CTRL, (2) WT-DSS, and (3) WT-DSS+Wy14643 (MCE, cat#:50892-23-4).

    Techniques: Gene Expression, Western Blot, Expressing, Cell Culture

    L. johnsonii activates hepatic LXRα–SCD1 signaling to ameliorate liver injury and colitis. (a) Schematic diagram of the mouse experiment. (b) Relative expression of LXRα downstream target genes ( n =6). (c) Levels of LXRα–SCD1 signaling pathway-related proteins in mice liver ( n =3). (d) Hepatic immunohistochemistry staining showed increased protein expression (LXRα, SREBP1, FASN and SCD1) by culture supernatant of L. johnsonii (Ljsup) ( n =3). (e) Relative abundance of liver LPC species altered by Ljsup ( n =5–6). (f) Serum LPS, TC and TG concentrations ( n =6). (g) Correlation analysis of differential LPC and LPE species with the serum TC, TG concentrations and hepatic SCD1 protein expression. (h, i) Body weight changes and disease activity index (DAI) during the experiment ( n =6). (j) Colon length, spleen and cecum index on day 8 ( n =6). (k) Representative H&E and AB/PAS staining of distal colon sections (scale bar, 100 µm) ( n =3). (l) Ljsup supplementation reduced the relative expression of colonic inflammatory cytokines ( n =6). (m) Ljsup supplementation increased the relative expression of colonic ZO-1 ( n =6). *, # p < 0.05, **, ## p < 0.01, ***, ### p < 0.001.

    Journal: Gut Microbes

    Article Title: Lactobacillus johnsonii mediates the protective effects of pristimerin against ulcerative colitis and concomitant liver injury through remodeling hepatic lipid metabolism via LXRα–SCD1 axis

    doi: 10.1080/19490976.2026.2701349

    Figure Lengend Snippet: L. johnsonii activates hepatic LXRα–SCD1 signaling to ameliorate liver injury and colitis. (a) Schematic diagram of the mouse experiment. (b) Relative expression of LXRα downstream target genes ( n =6). (c) Levels of LXRα–SCD1 signaling pathway-related proteins in mice liver ( n =3). (d) Hepatic immunohistochemistry staining showed increased protein expression (LXRα, SREBP1, FASN and SCD1) by culture supernatant of L. johnsonii (Ljsup) ( n =3). (e) Relative abundance of liver LPC species altered by Ljsup ( n =5–6). (f) Serum LPS, TC and TG concentrations ( n =6). (g) Correlation analysis of differential LPC and LPE species with the serum TC, TG concentrations and hepatic SCD1 protein expression. (h, i) Body weight changes and disease activity index (DAI) during the experiment ( n =6). (j) Colon length, spleen and cecum index on day 8 ( n =6). (k) Representative H&E and AB/PAS staining of distal colon sections (scale bar, 100 µm) ( n =3). (l) Ljsup supplementation reduced the relative expression of colonic inflammatory cytokines ( n =6). (m) Ljsup supplementation increased the relative expression of colonic ZO-1 ( n =6). *, # p < 0.05, **, ## p < 0.01, ***, ### p < 0.001.

    Article Snippet: Animal experiment 6 : PPARα KO-induced increase in hepatic SCD1 expression protected against colitis study, male 129/Sv wild-type mice (WT) were randomly classified into three groups ( n =5): (1) WT-CTRL, (2) WT-DSS, and (3) WT-DSS+Wy14643 (MCE, cat#:50892-23-4).

    Techniques: Expressing, Immunohistochemistry, Staining, Activity Assay

    SR9238 abolishes the liver protection and anti-colitis effects of L. johnsonii . (a) Relative mRNA levels of SREBF1, FASN and SCD1 in HepG2 cells pretreated with insulin (10 µg/ml) for 7 d, followed by 2 µM, 10 µM, and 20 µM SR9238 treatment ( n =3). (b) Schematic diagram of the mouse experiment. (c) Relative expression levels of hepatic SREBF1, FASN and SCD1 in mice ( n =6). (d) Representative images of mice colon, liver and spleen. (e) Masson's trichrome staining showed increased collagen in liver sections (scale bar, 100 µm) ( n =3). (f) Serum TG and TC concentrations ( n =6). (g) Oil Red O staining showed incereased lipid droplet accumulation (scale bar, 100 µm) ( n =3). (h, i) Body weight changes and disease activity index (DAI) changes during the experiment ( n =6). (j) Colon length, spleen and cecum index ( n =6). (k) Representative H&E and AB/PAS staining of distal colon sections (scale bar, 100 µm) ( n =3). (l) SR9238 reduced the relative expression of claudin and occludin in colon tissue ( n =5). *, # p < 0.05, **, ## p < 0.01, ***, ### p < 0.001.

    Journal: Gut Microbes

    Article Title: Lactobacillus johnsonii mediates the protective effects of pristimerin against ulcerative colitis and concomitant liver injury through remodeling hepatic lipid metabolism via LXRα–SCD1 axis

    doi: 10.1080/19490976.2026.2701349

    Figure Lengend Snippet: SR9238 abolishes the liver protection and anti-colitis effects of L. johnsonii . (a) Relative mRNA levels of SREBF1, FASN and SCD1 in HepG2 cells pretreated with insulin (10 µg/ml) for 7 d, followed by 2 µM, 10 µM, and 20 µM SR9238 treatment ( n =3). (b) Schematic diagram of the mouse experiment. (c) Relative expression levels of hepatic SREBF1, FASN and SCD1 in mice ( n =6). (d) Representative images of mice colon, liver and spleen. (e) Masson's trichrome staining showed increased collagen in liver sections (scale bar, 100 µm) ( n =3). (f) Serum TG and TC concentrations ( n =6). (g) Oil Red O staining showed incereased lipid droplet accumulation (scale bar, 100 µm) ( n =3). (h, i) Body weight changes and disease activity index (DAI) changes during the experiment ( n =6). (j) Colon length, spleen and cecum index ( n =6). (k) Representative H&E and AB/PAS staining of distal colon sections (scale bar, 100 µm) ( n =3). (l) SR9238 reduced the relative expression of claudin and occludin in colon tissue ( n =5). *, # p < 0.05, **, ## p < 0.01, ***, ### p < 0.001.

    Article Snippet: Animal experiment 6 : PPARα KO-induced increase in hepatic SCD1 expression protected against colitis study, male 129/Sv wild-type mice (WT) were randomly classified into three groups ( n =5): (1) WT-CTRL, (2) WT-DSS, and (3) WT-DSS+Wy14643 (MCE, cat#:50892-23-4).

    Techniques: Expressing, Staining, Activity Assay

    CORT aggravates colitis with liver injury through the LXRα‒SCD1 axis. (a) Oil Red O staining of AML12 cells treated with 2 µM, 10 µM, and 50 µM CORT. (b) Schematic diagram of the mouse experiment. (c) Protein levels of hepatic CD36, LXRα, FASN, and SCD1 in mice. (d) Representative immunohistochemical staining revealed the decreased protein expression (LXRα, FASN, SCD1, and CD36) in mice ( n =3). (e) Representative images of mice colon, liver and spleen. (f) Representative H&E, Masson's trichrome and Oil Red staining of liver sections (scale bar, 100 µm) ( n =3). (g) Serum TG and TC concentrations ( n =6). (h, i) Body weight changes and disease activity index (DAI) during the experiment ( n =6). (j) CORT reduced colon length ( n =6). (k) Representative H&E and AB/PAS staining of distal colon sections (scale bar, 100 µm) ( n =3). (l) Schematic diagram of the mouse experiment. (m, n) Relative mRNA levels of LXRα target genes. (o) Levels of LXRα signaling pathway-related proteins in mouse liver. (p) Serum TG and TC concentrations ( n =6). (q) Disease activity index (DAI) changes during the experiment ( n =6). (r) Colon length on day 12. * p < 0.05, ** p < 0.01, *** p < 0.001. ns, not significant ( p > 0.05).

    Journal: Gut Microbes

    Article Title: Lactobacillus johnsonii mediates the protective effects of pristimerin against ulcerative colitis and concomitant liver injury through remodeling hepatic lipid metabolism via LXRα–SCD1 axis

    doi: 10.1080/19490976.2026.2701349

    Figure Lengend Snippet: CORT aggravates colitis with liver injury through the LXRα‒SCD1 axis. (a) Oil Red O staining of AML12 cells treated with 2 µM, 10 µM, and 50 µM CORT. (b) Schematic diagram of the mouse experiment. (c) Protein levels of hepatic CD36, LXRα, FASN, and SCD1 in mice. (d) Representative immunohistochemical staining revealed the decreased protein expression (LXRα, FASN, SCD1, and CD36) in mice ( n =3). (e) Representative images of mice colon, liver and spleen. (f) Representative H&E, Masson's trichrome and Oil Red staining of liver sections (scale bar, 100 µm) ( n =3). (g) Serum TG and TC concentrations ( n =6). (h, i) Body weight changes and disease activity index (DAI) during the experiment ( n =6). (j) CORT reduced colon length ( n =6). (k) Representative H&E and AB/PAS staining of distal colon sections (scale bar, 100 µm) ( n =3). (l) Schematic diagram of the mouse experiment. (m, n) Relative mRNA levels of LXRα target genes. (o) Levels of LXRα signaling pathway-related proteins in mouse liver. (p) Serum TG and TC concentrations ( n =6). (q) Disease activity index (DAI) changes during the experiment ( n =6). (r) Colon length on day 12. * p < 0.05, ** p < 0.01, *** p < 0.001. ns, not significant ( p > 0.05).

    Article Snippet: Animal experiment 6 : PPARα KO-induced increase in hepatic SCD1 expression protected against colitis study, male 129/Sv wild-type mice (WT) were randomly classified into three groups ( n =5): (1) WT-CTRL, (2) WT-DSS, and (3) WT-DSS+Wy14643 (MCE, cat#:50892-23-4).

    Techniques: Staining, Immunohistochemical staining, Expressing, Activity Assay

    Protein expression levels ( A , H ) including ( B ) PPARγ, ( C ) Fabp4, ( D ) CD36, ( E ) SREBP-1c, ( F ) ADIPOQ, ( G ) SCD-1, ( I ) TLR4, ( J ) IKKβ, and ( K ) p-P65 in liver tissues among NCD, HFCD, and HFCD + HB-1. Data were expressed as mean ± SD ( n = 3) based on Dunnett’s test. ** indicated p < 0.01, *** indicated p < 0.001, **** indicated p < 0.0001.

    Journal: Foods

    Article Title: Chemical Composition Analysis of Highland Barley ( Hordeum vulgare L.) with Different Modification Methods and Lipid Metabolism Mechanism Analysis of Highland Barley with Microwave Fluidization Modification

    doi: 10.3390/foods15081396

    Figure Lengend Snippet: Protein expression levels ( A , H ) including ( B ) PPARγ, ( C ) Fabp4, ( D ) CD36, ( E ) SREBP-1c, ( F ) ADIPOQ, ( G ) SCD-1, ( I ) TLR4, ( J ) IKKβ, and ( K ) p-P65 in liver tissues among NCD, HFCD, and HFCD + HB-1. Data were expressed as mean ± SD ( n = 3) based on Dunnett’s test. ** indicated p < 0.01, *** indicated p < 0.001, **** indicated p < 0.0001.

    Article Snippet: The specific antibody concentrations used in this study were as follows: anti-rabbit antibodies against Peroxisome proliferator-activated receptor γ (PPARγ) (1:1000, 58 kDa, Affinity, 16643-1-AP), FABP4 (1:1000, 15 kDa, Affinity, DF6035), CD36 (1:1000, 88 kDa, Affinity, DF13262), SREBP-1c (1:1000, 122 kDa, Affinity, AF6283), ADIPOQ (1:1000, 26 kDa, Affinity, DF7000), SCD-1 (1:1000, 41 kDa, Bioss, bs-3787R), p-P65 (1:1000, 65 kDa, Affinity, AF2006, Serine Ser536), TLR4 (1:1000, 100 kDa, Affinity, AF7017), IKKβ (1:1000, 87 kDa, Affinity, AF6010), and GAPDH (1:1000, 37 kDa, Xianzhi Biotech, AB-P-R 001).

    Techniques: Expressing

    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.

    Journal: Stem Cells Translational Medicine

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

    doi: 10.1093/stcltm/szag016

    Figure Lengend 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.

    Article Snippet: Primary antibodies specific for the following proteins were obtained from Cell Signaling Technology: ACC-1 (#3676), SCD1 (#2794), FASN (#3180), p-AKT (#4060), and AKT (#9272).

    Techniques: 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.

    Journal: Stem Cells Translational Medicine

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

    doi: 10.1093/stcltm/szag016

    Figure Lengend 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.

    Article Snippet: Primary antibodies specific for the following proteins were obtained from Cell Signaling Technology: ACC-1 (#3676), SCD1 (#2794), FASN (#3180), p-AKT (#4060), and AKT (#9272).

    Techniques: Transplantation Assay, Staining, Western Blot