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socs3 primary antibody  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology socs3 primary antibody
    Socs3 Primary Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 431 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/socs3+antibody/pm41861528-96-38-42?v=Santa+Cruz+Biotechnology
    Average 94 stars, based on 431 article reviews
    socs3 primary antibody - by Bioz Stars, 2026-07
    94/100 stars

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    RAW264.7 cells were cultured in αKG-supplemented medium, treated with the STAT3 inhibitor Stattic, and subsequently stimulated with S. aureus . A: Protein expression levels of the JAK1/STAT3 signaling pathway and its negative regulator <t>SOCS3</t> were detected in the Control, αKG, and αKG + S. au groups. B-I: Relative mRNA expression of M2 and M1 marker genes across the four experimental groups. J-L: Inflammatory cytokine levels and NF-κB signaling pathway activity in the Control, αKG, αKG + S. au , and αKG + S. au +Stattic groups. M: Expression levels of the JAK1/STAT3 signaling pathway across the four experimental groups. The data are presented as mean ± SD. One-way analysis of variance was performed for statistical analysis. * P < 0.05, ** P < 0.01 and *** P < 0.001 indicate significance from each group. ns, no significance.
    Socs3, supplied by Bioss, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology socs3 primary antibody
    RAW264.7 cells were cultured in αKG-supplemented medium, treated with the STAT3 inhibitor Stattic, and subsequently stimulated with S. aureus . A: Protein expression levels of the JAK1/STAT3 signaling pathway and its negative regulator <t>SOCS3</t> were detected in the Control, αKG, and αKG + S. au groups. B-I: Relative mRNA expression of M2 and M1 marker genes across the four experimental groups. J-L: Inflammatory cytokine levels and NF-κB signaling pathway activity in the Control, αKG, αKG + S. au , and αKG + S. au +Stattic groups. M: Expression levels of the JAK1/STAT3 signaling pathway across the four experimental groups. The data are presented as mean ± SD. One-way analysis of variance was performed for statistical analysis. * P < 0.05, ** P < 0.01 and *** P < 0.001 indicate significance from each group. ns, no significance.
    Socs3 Primary Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/socs3+antibody/pm41861528-96-38-42?v=Santa+Cruz+Biotechnology
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    Proteintech antibodies against socs3
    The molecular mechanism of STAT3 signaling pathway regulated by AKR1C3 in CCA. (A) After treatment with IL-6, the expression levels of proliferation, invasion, drug resistance, glycolysis, and STAT3 signaling-associated proteins were detected by Western blot in QBC939 cells. IL-6, 30 ng/ml. (B) The mRNA expression levels of the SOCSs family in QBC939 cells after AKR1C3 knockdown were detected by Q-PCR. * P < 0.05 (C) The protein expression levels of SOCS1 and <t>SOCS3</t> in CCA cells after AKR1C3 knockdown and overexpression were measured by Western blot. (D) Western blot was performed to assess the ubiquitination degradation of SOCS1 in shAKR1C3- or shCtrl-transfected QBC939 cells treated with 50 µM cyclohexane (CHX) at different times. (E) Co-IP assay was conducted to investigate the protein interaction between AKR1C3 and SOCS1 in QBC939 cells.
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    Proteintech antibodies against socs3 68631s
    The molecular mechanism of STAT3 signaling pathway regulated by AKR1C3 in CCA. (A) After treatment with IL-6, the expression levels of proliferation, invasion, drug resistance, glycolysis, and STAT3 signaling-associated proteins were detected by Western blot in QBC939 cells. IL-6, 30 ng/ml. (B) The mRNA expression levels of the SOCSs family in QBC939 cells after AKR1C3 knockdown were detected by Q-PCR. * P < 0.05 (C) The protein expression levels of SOCS1 and <t>SOCS3</t> in CCA cells after AKR1C3 knockdown and overexpression were measured by Western blot. (D) Western blot was performed to assess the ubiquitination degradation of SOCS1 in shAKR1C3- or shCtrl-transfected QBC939 cells treated with 50 µM cyclohexane (CHX) at different times. (E) Co-IP assay was conducted to investigate the protein interaction between AKR1C3 and SOCS1 in QBC939 cells.
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    <t>Socs3</t> expression is elevated in HFpEF hearts and reduced after NanoAM treatment. (A,B) Volcano plots illustrate differential gene expression between groups: HF versus NC (A) , and HFi versus HF (B,C) Venn diagrams display the number of genes with opposite expression patterns in the HFi versus HF comparison relative to the HF versus NC comparison. (D) A Heatmap presents the relative expression levels of the 48 genes across three groups. (E) Interaction network between the 48 genes and insulin resistance (IR)-related genes enriched in , identifying Socs3 as the key overlapping gene.
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    <t>Socs3</t> expression is elevated in HFpEF hearts and reduced after NanoAM treatment. (A,B) Volcano plots illustrate differential gene expression between groups: HF versus NC (A) , and HFi versus HF (B,C) Venn diagrams display the number of genes with opposite expression patterns in the HFi versus HF comparison relative to the HF versus NC comparison. (D) A Heatmap presents the relative expression levels of the 48 genes across three groups. (E) Interaction network between the 48 genes and insulin resistance (IR)-related genes enriched in , identifying Socs3 as the key overlapping gene.
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    Santa Cruz Biotechnology socs3
    <t>Socs3</t> expression is elevated in HFpEF hearts and reduced after NanoAM treatment. (A,B) Volcano plots illustrate differential gene expression between groups: HF versus NC (A) , and HFi versus HF (B,C) Venn diagrams display the number of genes with opposite expression patterns in the HFi versus HF comparison relative to the HF versus NC comparison. (D) A Heatmap presents the relative expression levels of the 48 genes across three groups. (E) Interaction network between the 48 genes and insulin resistance (IR)-related genes enriched in , identifying Socs3 as the key overlapping gene.
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    Proteintech protein a g magnetic beads
    <t>Socs3</t> expression is elevated in HFpEF hearts and reduced after NanoAM treatment. (A,B) Volcano plots illustrate differential gene expression between groups: HF versus NC (A) , and HFi versus HF (B,C) Venn diagrams display the number of genes with opposite expression patterns in the HFi versus HF comparison relative to the HF versus NC comparison. (D) A Heatmap presents the relative expression levels of the 48 genes across three groups. (E) Interaction network between the 48 genes and insulin resistance (IR)-related genes enriched in , identifying Socs3 as the key overlapping gene.
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    RAW264.7 cells were cultured in αKG-supplemented medium, treated with the STAT3 inhibitor Stattic, and subsequently stimulated with S. aureus . A: Protein expression levels of the JAK1/STAT3 signaling pathway and its negative regulator SOCS3 were detected in the Control, αKG, and αKG + S. au groups. B-I: Relative mRNA expression of M2 and M1 marker genes across the four experimental groups. J-L: Inflammatory cytokine levels and NF-κB signaling pathway activity in the Control, αKG, αKG + S. au , and αKG + S. au +Stattic groups. M: Expression levels of the JAK1/STAT3 signaling pathway across the four experimental groups. The data are presented as mean ± SD. One-way analysis of variance was performed for statistical analysis. * P < 0.05, ** P < 0.01 and *** P < 0.001 indicate significance from each group. ns, no significance.

    Journal: PLOS Pathogens

    Article Title: Glutamine alleviates Staphylococcus aureus -induced mastitis by modulating macrophage polarisation

    doi: 10.1371/journal.ppat.1014053

    Figure Lengend Snippet: RAW264.7 cells were cultured in αKG-supplemented medium, treated with the STAT3 inhibitor Stattic, and subsequently stimulated with S. aureus . A: Protein expression levels of the JAK1/STAT3 signaling pathway and its negative regulator SOCS3 were detected in the Control, αKG, and αKG + S. au groups. B-I: Relative mRNA expression of M2 and M1 marker genes across the four experimental groups. J-L: Inflammatory cytokine levels and NF-κB signaling pathway activity in the Control, αKG, αKG + S. au , and αKG + S. au +Stattic groups. M: Expression levels of the JAK1/STAT3 signaling pathway across the four experimental groups. The data are presented as mean ± SD. One-way analysis of variance was performed for statistical analysis. * P < 0.05, ** P < 0.01 and *** P < 0.001 indicate significance from each group. ns, no significance.

    Article Snippet: The specific primary antibodies used in the experiment included p65 (#8242, Cell Signaling Technology, USA), p-p65 (#3033, Cell Signaling Technology, America), IκB (AF5002, Affinity Biosciences, Jiangsu, China), p-IκB (AF2002, Affinity Biosciences, Jiangsu, China), ZO-1 (AF5145, Affinity Biosciences, Jiangsu, China), Occludin (DF7504, Affinity Biosciences, Jiangsu, China), Claudin-3 (AF0129, Affinity Biosciences, Jiangsu, China), ATG5 (bsm-52596R, Bioss, Woburn, MA, USA), LC3-I/LC3-II (AF5402, Affinity Biosciences, Jiangsu, China), p62 (ab91526, Abcam plc, Cam bridge, UK), SOCS3 (bs-0580R, Bioss, Woburn, MA, USA), JAK1 (bs-1439R , Bioss, Woburn, MA, USA), p-JAK1 (bs-3238R, Bioss, Woburn, MA, USA), STAT3 (AF6294, Affinity Biosciences, Jiangsu, China), p-STAT3 (AF3293, Affinity Biosciences, Jiangsu, China) and β-actin (T0022, Affinity Biosciences, Jiangsu, China).

    Techniques: Cell Culture, Expressing, Control, Marker, Activity Assay

    The molecular mechanism of STAT3 signaling pathway regulated by AKR1C3 in CCA. (A) After treatment with IL-6, the expression levels of proliferation, invasion, drug resistance, glycolysis, and STAT3 signaling-associated proteins were detected by Western blot in QBC939 cells. IL-6, 30 ng/ml. (B) The mRNA expression levels of the SOCSs family in QBC939 cells after AKR1C3 knockdown were detected by Q-PCR. * P < 0.05 (C) The protein expression levels of SOCS1 and SOCS3 in CCA cells after AKR1C3 knockdown and overexpression were measured by Western blot. (D) Western blot was performed to assess the ubiquitination degradation of SOCS1 in shAKR1C3- or shCtrl-transfected QBC939 cells treated with 50 µM cyclohexane (CHX) at different times. (E) Co-IP assay was conducted to investigate the protein interaction between AKR1C3 and SOCS1 in QBC939 cells.

    Journal: Scientific Reports

    Article Title: Cancer-Associated fibroblasts regulate the development of cholangiocarcinoma through IL-6/STAT3/AKR1C3 signaling axis

    doi: 10.1038/s41598-026-37583-y

    Figure Lengend Snippet: The molecular mechanism of STAT3 signaling pathway regulated by AKR1C3 in CCA. (A) After treatment with IL-6, the expression levels of proliferation, invasion, drug resistance, glycolysis, and STAT3 signaling-associated proteins were detected by Western blot in QBC939 cells. IL-6, 30 ng/ml. (B) The mRNA expression levels of the SOCSs family in QBC939 cells after AKR1C3 knockdown were detected by Q-PCR. * P < 0.05 (C) The protein expression levels of SOCS1 and SOCS3 in CCA cells after AKR1C3 knockdown and overexpression were measured by Western blot. (D) Western blot was performed to assess the ubiquitination degradation of SOCS1 in shAKR1C3- or shCtrl-transfected QBC939 cells treated with 50 µM cyclohexane (CHX) at different times. (E) Co-IP assay was conducted to investigate the protein interaction between AKR1C3 and SOCS1 in QBC939 cells.

    Article Snippet: Antibodies against SOCS3 (68631 S) and PFK-1 (55028-1-AP) were obtained from Proteintech. (Hubei, China).

    Techniques: Expressing, Western Blot, Knockdown, Over Expression, Ubiquitin Proteomics, Transfection, Co-Immunoprecipitation Assay

    Socs3 expression is elevated in HFpEF hearts and reduced after NanoAM treatment. (A,B) Volcano plots illustrate differential gene expression between groups: HF versus NC (A) , and HFi versus HF (B,C) Venn diagrams display the number of genes with opposite expression patterns in the HFi versus HF comparison relative to the HF versus NC comparison. (D) A Heatmap presents the relative expression levels of the 48 genes across three groups. (E) Interaction network between the 48 genes and insulin resistance (IR)-related genes enriched in , identifying Socs3 as the key overlapping gene.

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: Bioinspired cardiac-targeted metal-organic framework nanozyme for modulating inflammatory responses in heart failure with preserved ejection fraction

    doi: 10.3389/fbioe.2026.1744643

    Figure Lengend Snippet: Socs3 expression is elevated in HFpEF hearts and reduced after NanoAM treatment. (A,B) Volcano plots illustrate differential gene expression between groups: HF versus NC (A) , and HFi versus HF (B,C) Venn diagrams display the number of genes with opposite expression patterns in the HFi versus HF comparison relative to the HF versus NC comparison. (D) A Heatmap presents the relative expression levels of the 48 genes across three groups. (E) Interaction network between the 48 genes and insulin resistance (IR)-related genes enriched in , identifying Socs3 as the key overlapping gene.

    Article Snippet: Antibodies against IRS1-Ser307 (Proteintech, 85238-1-RR, dilution 1:5000), P-AKT1-T308+AKT2-T309+AKT3-T305 (ABclonal, AP1266, dilution 1:800), SOCS3 (Proteintech, 66797-1-Ig, dilution 1:20,000), and GAPDH (Servicebio, GB15002-100, dilution 1:8000) were used.

    Techniques: Expressing, Gene Expression, Comparison

    NanoAM regulates the SOCS3-IRS1-AKT2 axis to improve insulin resistance. (A,B) WB analysis of insulin resistance-related proteins in heart tissue (n = 6). (C) The Socs3 mRNA expression levels in heart tissues were determined by qPCR. (D) Immunofluorescence staining of GLUT4 in cardiac tissues. Scale bar, 10 µm. (E) Fluorescence intensity quantification of GLUT4 was shown. (F–I) The Inflammatory factors (IL-6,TNF-α,IL-1β,CRP) mRNA expression levels in heart tissues were determined by qPCR. (J,K) Serum levels of IL-6 and hs-CRP measured by ELISA. Data are showed as mean ± SD and analyzed using one-way ANOVA followed by Tukey’s post hoc test; *p < 0.05, ***p < 0.001.

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: Bioinspired cardiac-targeted metal-organic framework nanozyme for modulating inflammatory responses in heart failure with preserved ejection fraction

    doi: 10.3389/fbioe.2026.1744643

    Figure Lengend Snippet: NanoAM regulates the SOCS3-IRS1-AKT2 axis to improve insulin resistance. (A,B) WB analysis of insulin resistance-related proteins in heart tissue (n = 6). (C) The Socs3 mRNA expression levels in heart tissues were determined by qPCR. (D) Immunofluorescence staining of GLUT4 in cardiac tissues. Scale bar, 10 µm. (E) Fluorescence intensity quantification of GLUT4 was shown. (F–I) The Inflammatory factors (IL-6,TNF-α,IL-1β,CRP) mRNA expression levels in heart tissues were determined by qPCR. (J,K) Serum levels of IL-6 and hs-CRP measured by ELISA. Data are showed as mean ± SD and analyzed using one-way ANOVA followed by Tukey’s post hoc test; *p < 0.05, ***p < 0.001.

    Article Snippet: Antibodies against IRS1-Ser307 (Proteintech, 85238-1-RR, dilution 1:5000), P-AKT1-T308+AKT2-T309+AKT3-T305 (ABclonal, AP1266, dilution 1:800), SOCS3 (Proteintech, 66797-1-Ig, dilution 1:20,000), and GAPDH (Servicebio, GB15002-100, dilution 1:8000) were used.

    Techniques: Expressing, Immunofluorescence, Staining, Fluorescence, Enzyme-linked Immunosorbent Assay