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anti scd1  (Cell Signaling Technology Inc)


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    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/anti+scd1/SCD1+Rabbit+mAb/pm41935215-265-21-22
    Average 95 stars, based on 224 article reviews
    anti scd1 - by Bioz Stars, 2026-10
    95/100 stars

    Images

    Related Articles

    Western Blot:

    Article Title: Free fatty acids increase basal glucose uptake by adipocytes leveling it to insulin-stimulated uptake
    Article Snippet: .. The following primary antibodies were used for western blotting: anti-CPT1A (#15184, Proteintech, USA), anti-CPT1B (#22170, Proteintech, USA), anti-SCD1 (#2438, CellSignaling, USA), anti-UCP1 (#14670, CellSignaling, USA), and anti-vinculin (#9131, Sigma, USA). .. As secondary antibodies, goat anti-rabbit IgG (#ab6721, Abcam, USA) or goat anti-mouse IgG (#ab97023, Abcam, USA) conjugated with horseradish peroxidase were used.

    Blocking Assay:

    Article Title: Proteomic analysis reveals the pro-proliferative role of the LIN28B/HMGA2 axis in hepatoblastoma.
    Article Snippet: immature hepatocytes.. HB can be divided into three pathological types based on the different proportions of epithelial cells, namely the wholly epithelial, mixed epithelial, and mesenchymal types [3].Clinical studies have shown that HB is associated with certain genetic syndromes, such as familial adenomatous polyposis, Beckwith-Wiedemann syndrome, and trisomy 18 syndrome [4–6].. The specific mechanisms of the tumorigenesis and development of HB remain unclear, but studies have shown that it may be promoted by aberrant activation of several signaling pathways and high expression of specific oncogenes.

    Incubation:

    Article Title: Proteomic analysis reveals the pro-proliferative role of the LIN28B/HMGA2 axis in hepatoblastoma.
    Article Snippet: immature hepatocytes.. HB can be divided into three pathological types based on the different proportions of epithelial cells, namely the wholly epithelial, mixed epithelial, and mesenchymal types [3].Clinical studies have shown that HB is associated with certain genetic syndromes, such as familial adenomatous polyposis, Beckwith-Wiedemann syndrome, and trisomy 18 syndrome [4–6].. The specific mechanisms of the tumorigenesis and development of HB remain unclear, but studies have shown that it may be promoted by aberrant activation of several signaling pathways and high expression of specific oncogenes.



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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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    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, <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.
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    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, <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.
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    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, <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.
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    Image Search Results


    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