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mouse monoclonal anti ap2 beta  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology mouse monoclonal anti ap2 beta
    Mouse Monoclonal Anti Ap2 Beta, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 41 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+anti+ap2+monoclonal+antibody/pm38167340-364-18-22?v=Santa+Cruz+Biotechnology
    Average 93 stars, based on 41 article reviews
    mouse monoclonal anti ap2 beta - by Bioz Stars, 2026-08
    93/100 stars

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    Santa Cruz Biotechnology mouse monoclonal antibodies for ap2
    PSE inhibits adipogenesis in 3T3-L1 adipocytes. 3T3-L1 cells were seeded and induced to differentiation in the presence of DMSO (vehicle control), resveratrol (20–40 μM) or PSE (50–200 μg/mL) for 10 days: ( A ) TG accumulation in 96-well culture plates was visualized by ORO staining; ( B ) extracted ORO staining was quantified (OD 500 nm); ( C ) representative images from three separate experiments (magnified 4×); ( D ) adipogenic gene expression of PPARγ, <t>aP2,</t> C/EBP α, and Fas by qPCR; ( E ) adipogenic protein expressions of PPARγ, aP2, phosphor-specific, or total antibodies targeting AMPK and β-actin by Western blot analysis. All values are presented as the mean ±S.E.M. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001 compared with the vehicle control (DMSO treated cells) by one-way ANOVA with Bonferroni’s comparison test. +; treatment, -; non-treatment.
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    Santa Cruz Biotechnology mouse anti-adipocyte protein 2 (ap2) monoclonal antibody
    PSE inhibits adipogenesis in 3T3-L1 adipocytes. 3T3-L1 cells were seeded and induced to differentiation in the presence of DMSO (vehicle control), resveratrol (20–40 μM) or PSE (50–200 μg/mL) for 10 days: ( A ) TG accumulation in 96-well culture plates was visualized by ORO staining; ( B ) extracted ORO staining was quantified (OD 500 nm); ( C ) representative images from three separate experiments (magnified 4×); ( D ) adipogenic gene expression of PPARγ, <t>aP2,</t> C/EBP α, and Fas by qPCR; ( E ) adipogenic protein expressions of PPARγ, aP2, phosphor-specific, or total antibodies targeting AMPK and β-actin by Western blot analysis. All values are presented as the mean ±S.E.M. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001 compared with the vehicle control (DMSO treated cells) by one-way ANOVA with Bonferroni’s comparison test. +; treatment, -; non-treatment.
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    Image Search Results


    Journal: eLife

    Article Title: Glycosylphosphatidylinositol biosynthesis and remodeling are required for neural tube closure, heart development, and cranial neural crest cell survival

    doi: 10.7554/eLife.45248

    Figure Lengend Snippet:

    Article Snippet: Antibody , mouse monoclonal anti-AP2 , Developmental Studies Hybridoma Bank , DSHB: #3B5 supernatant RRID: AB_528084 , (1:20).

    Techniques: Sequencing, RNA Sequencing, Recombinant, Control, Software, Plasmid Preparation, CRISPR, Transfection, Construct

    Journal: Cell Stem Cell

    Article Title: Naive stem cell blastocyst model captures human embryo lineage segregation

    doi: 10.1016/j.stem.2021.04.031

    Figure Lengend Snippet:

    Article Snippet: Mouse monoclonal anti-AP2 gamma , Santa Cruz , Cat# sc-12762, RRID: AB_667770.

    Techniques: Recombinant, Cell Attachment Assay, Software

    Journal: eLife

    Article Title: Misfolded GPI-anchored proteins are escorted through the secretory pathway by ER-derived factors

    doi: 10.7554/eLife.46740

    Figure Lengend Snippet:

    Article Snippet: Antibody , mouse monoclonal anti-alpha adaptin (AP2) , BD Biosciences , Cat #610502, RRID: AB_397868 , (1:3000).

    Techniques: CRISPR, Recombinant, Sequencing, Plasmid Preparation, Expressing, Dominant Negative Mutation, Mutagenesis, Negative Control, Purification, Affinity Chromatography, Labeling

    PSE inhibits adipogenesis in 3T3-L1 adipocytes. 3T3-L1 cells were seeded and induced to differentiation in the presence of DMSO (vehicle control), resveratrol (20–40 μM) or PSE (50–200 μg/mL) for 10 days: ( A ) TG accumulation in 96-well culture plates was visualized by ORO staining; ( B ) extracted ORO staining was quantified (OD 500 nm); ( C ) representative images from three separate experiments (magnified 4×); ( D ) adipogenic gene expression of PPARγ, aP2, C/EBP α, and Fas by qPCR; ( E ) adipogenic protein expressions of PPARγ, aP2, phosphor-specific, or total antibodies targeting AMPK and β-actin by Western blot analysis. All values are presented as the mean ±S.E.M. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001 compared with the vehicle control (DMSO treated cells) by one-way ANOVA with Bonferroni’s comparison test. +; treatment, -; non-treatment.

    Journal: International Journal of Molecular Sciences

    Article Title: Peanut Sprout Extracts Attenuate Triglyceride Accumulation by Promoting Mitochondrial Fatty Acid Oxidation in Adipocytes

    doi: 10.3390/ijms20051216

    Figure Lengend Snippet: PSE inhibits adipogenesis in 3T3-L1 adipocytes. 3T3-L1 cells were seeded and induced to differentiation in the presence of DMSO (vehicle control), resveratrol (20–40 μM) or PSE (50–200 μg/mL) for 10 days: ( A ) TG accumulation in 96-well culture plates was visualized by ORO staining; ( B ) extracted ORO staining was quantified (OD 500 nm); ( C ) representative images from three separate experiments (magnified 4×); ( D ) adipogenic gene expression of PPARγ, aP2, C/EBP α, and Fas by qPCR; ( E ) adipogenic protein expressions of PPARγ, aP2, phosphor-specific, or total antibodies targeting AMPK and β-actin by Western blot analysis. All values are presented as the mean ±S.E.M. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001 compared with the vehicle control (DMSO treated cells) by one-way ANOVA with Bonferroni’s comparison test. +; treatment, -; non-treatment.

    Article Snippet: The mouse monoclonal antibodies for aP2 (sc-271529) were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

    Techniques: Control, Staining, Gene Expression, Western Blot, Comparison

    PSE inhibits adipogenesis in C3H10T1/2 mouse embryonic fibroblasts, adipocytes, and EMSCs. C3H10T1/2 cells were seeded and induced to differentiation in the presence of either DMSO (vehicle control) and PSE (5–100 μg/mL) for four days: ( A ) Triglyceride accumulation was visualized by Oil red-O staining and representative images from three separate experiments are shown in ( left ) (magnified 4×); extracted ORO staining was quantified (OD 500 nm) ( right ). Primary adipocytes were prepared from EMSC of Balb/c mice: ( B ) Phase contrast images of primary adipocytes were differentiated with or without PSE (25 μg/mL) for seven days (magnified 4×, scale bar = 400 μm); ( C ) adipogenic gene expression of PPARγ and aP2 by qPCR. * p < 0.05; ** p < 0.01; **** p < 0.0001 compared with the vehicle control (DMSO treated cells) by one-way ANOVA with Bonferroni’s comparison test or Student’s t-test. +; treatment, -; non-treatment.

    Journal: International Journal of Molecular Sciences

    Article Title: Peanut Sprout Extracts Attenuate Triglyceride Accumulation by Promoting Mitochondrial Fatty Acid Oxidation in Adipocytes

    doi: 10.3390/ijms20051216

    Figure Lengend Snippet: PSE inhibits adipogenesis in C3H10T1/2 mouse embryonic fibroblasts, adipocytes, and EMSCs. C3H10T1/2 cells were seeded and induced to differentiation in the presence of either DMSO (vehicle control) and PSE (5–100 μg/mL) for four days: ( A ) Triglyceride accumulation was visualized by Oil red-O staining and representative images from three separate experiments are shown in ( left ) (magnified 4×); extracted ORO staining was quantified (OD 500 nm) ( right ). Primary adipocytes were prepared from EMSC of Balb/c mice: ( B ) Phase contrast images of primary adipocytes were differentiated with or without PSE (25 μg/mL) for seven days (magnified 4×, scale bar = 400 μm); ( C ) adipogenic gene expression of PPARγ and aP2 by qPCR. * p < 0.05; ** p < 0.01; **** p < 0.0001 compared with the vehicle control (DMSO treated cells) by one-way ANOVA with Bonferroni’s comparison test or Student’s t-test. +; treatment, -; non-treatment.

    Article Snippet: The mouse monoclonal antibodies for aP2 (sc-271529) were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

    Techniques: Control, Staining, Gene Expression, Comparison

    PSE attenuates lipid accumulation in cultures of adipocytes by upregulating fatty acid oxidation and mitochondrial oxygen consumption. ( A ) Experimental scheme. 3T3-L1 were seeded on the second day before differentiation ( d-2 ) and induced to differentiation ( d0 , MDI: methyl isobutyl- xanthine, dexamethasone, and insulin). Keep 3T3-L1 cells differentiated into fully differentiated adipocytes until d7. Fully differentiated adipocytes ( d7 ) were incubated with PSE (25 μg/mL) for three days. ( B ) Lipogenic and fatty acid oxidation-related gene expression of PPARγ, aP2, PGC1α, CPT1, and PPARα as determined by qPCR. ( C ) Conversion of [ 3 H]-OA into [ 3 H]-H 2 O. ( D – F ) Oxygen consumption rate (OCR) in 3T3-L1 adipocytes treated with Veh (blue) and PSE (red) as determined by Seahorse extracellular analyzer. 3T3-L1 cells differentiated into fully differentiated adipocytes. Fully differentiated adipocytes ( d7 ) were incubated with PSE (25 μg/mL) for one day. Arrow indicates the addition of respiratory inhibitors of oligomycin (Oligo), carbonyl cyanide 4-trifluoromethoxy phenylhydrazone (FCCP) and a combination of antimycin A and rotenone (Rot/AA). ( G – H ) OCR in HepG2 cells treated with BSA (black), PA (blue), and PA + PSE (red) as determined by Seahorse extracellular analyzer. HepG2 cells were pre-incubated with PSE (50 μg/mL)for 48 h. BSA or 0.8 mM BSA-PA complex was loaded for 3 h. (I) Relative expressions of UCP1 and PGC1α by qPCR. Pre-treatment of the 3T3-L1 cell with PSE for 7 d during adipogenesis, followed by Bt2-cAMP stimulation for 6 h. All values are presented as the mean ±SEM. n.s. represents no significance. * p < 0.05; ** p < 0.01; *** p < 0.001 compared with the vehicle control (DMSO-treated cells) by Student’s t -test or one-way ANOVA with Bonferroni’s comparison test. Means that do not share a common superscript are significantly different as determined by one-way ANOVA with Bonferroni’s comparison test. ++ p < 0.01; +++ p < 0.001 compared with the vehicle control (DMSO treated cells) # p < 0.05; ## p < 0.01; ### p < 0.001 compared with PA-treated HepG2 cells by two-way ANOVA with Bonferroni’s comparison test. +; treatment, -; non-treatment.

    Journal: International Journal of Molecular Sciences

    Article Title: Peanut Sprout Extracts Attenuate Triglyceride Accumulation by Promoting Mitochondrial Fatty Acid Oxidation in Adipocytes

    doi: 10.3390/ijms20051216

    Figure Lengend Snippet: PSE attenuates lipid accumulation in cultures of adipocytes by upregulating fatty acid oxidation and mitochondrial oxygen consumption. ( A ) Experimental scheme. 3T3-L1 were seeded on the second day before differentiation ( d-2 ) and induced to differentiation ( d0 , MDI: methyl isobutyl- xanthine, dexamethasone, and insulin). Keep 3T3-L1 cells differentiated into fully differentiated adipocytes until d7. Fully differentiated adipocytes ( d7 ) were incubated with PSE (25 μg/mL) for three days. ( B ) Lipogenic and fatty acid oxidation-related gene expression of PPARγ, aP2, PGC1α, CPT1, and PPARα as determined by qPCR. ( C ) Conversion of [ 3 H]-OA into [ 3 H]-H 2 O. ( D – F ) Oxygen consumption rate (OCR) in 3T3-L1 adipocytes treated with Veh (blue) and PSE (red) as determined by Seahorse extracellular analyzer. 3T3-L1 cells differentiated into fully differentiated adipocytes. Fully differentiated adipocytes ( d7 ) were incubated with PSE (25 μg/mL) for one day. Arrow indicates the addition of respiratory inhibitors of oligomycin (Oligo), carbonyl cyanide 4-trifluoromethoxy phenylhydrazone (FCCP) and a combination of antimycin A and rotenone (Rot/AA). ( G – H ) OCR in HepG2 cells treated with BSA (black), PA (blue), and PA + PSE (red) as determined by Seahorse extracellular analyzer. HepG2 cells were pre-incubated with PSE (50 μg/mL)for 48 h. BSA or 0.8 mM BSA-PA complex was loaded for 3 h. (I) Relative expressions of UCP1 and PGC1α by qPCR. Pre-treatment of the 3T3-L1 cell with PSE for 7 d during adipogenesis, followed by Bt2-cAMP stimulation for 6 h. All values are presented as the mean ±SEM. n.s. represents no significance. * p < 0.05; ** p < 0.01; *** p < 0.001 compared with the vehicle control (DMSO-treated cells) by Student’s t -test or one-way ANOVA with Bonferroni’s comparison test. Means that do not share a common superscript are significantly different as determined by one-way ANOVA with Bonferroni’s comparison test. ++ p < 0.01; +++ p < 0.001 compared with the vehicle control (DMSO treated cells) # p < 0.05; ## p < 0.01; ### p < 0.001 compared with PA-treated HepG2 cells by two-way ANOVA with Bonferroni’s comparison test. +; treatment, -; non-treatment.

    Article Snippet: The mouse monoclonal antibodies for aP2 (sc-271529) were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

    Techniques: Incubation, Gene Expression, Control, Comparison