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anti rrbp1  (Proteintech)


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    Proteintech anti rrbp1
    <t>RRBP1</t> inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with <t>an</t> <t>anti-RRBP1</t> antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.
    Anti Rrbp1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Targeting RRBP1 reverses immune evasion and enhances immunotherapy efficacy via the CXCL10-CXCR3 axis in bladder cancer"

    Article Title: Targeting RRBP1 reverses immune evasion and enhances immunotherapy efficacy via the CXCL10-CXCR3 axis in bladder cancer

    Journal: Journal for Immunotherapy of Cancer

    doi: 10.1136/jitc-2025-013809

    RRBP1 inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with an anti-RRBP1 antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.
    Figure Legend Snippet: RRBP1 inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with an anti-RRBP1 antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.

    Techniques Used: Inhibition, Protein-Protein interactions, Expressing, Immunohistochemistry, Enzyme-linked Immunosorbent Assay, Binding Assay, Knockdown, Two Tailed Test, Real-time Polymerase Chain Reaction



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    <t>RRBP1</t> inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with <t>an</t> <t>anti-RRBP1</t> antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.
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    <t>RRBP1</t> inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with <t>an</t> <t>anti-RRBP1</t> antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.
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    <t>RRBP1</t> inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with <t>an</t> <t>anti-RRBP1</t> antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.
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    <t>RRBP1</t> inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with <t>an</t> <t>anti-RRBP1</t> antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.
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    <t>RRBP1</t> inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with <t>an</t> <t>anti-RRBP1</t> antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.
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    <t>RRBP1</t> inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with <t>an</t> <t>anti-RRBP1</t> antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.
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    <t>RRBP1</t> inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with <t>an</t> <t>anti-RRBP1</t> antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.
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    Image Search Results


    RRBP1 inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with an anti-RRBP1 antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.

    Journal: Journal for Immunotherapy of Cancer

    Article Title: Targeting RRBP1 reverses immune evasion and enhances immunotherapy efficacy via the CXCL10-CXCR3 axis in bladder cancer

    doi: 10.1136/jitc-2025-013809

    Figure Lengend Snippet: RRBP1 inhibition increases the CXCL10 mRNA stability in BC. ( A ) The volcano plot showed that differentially expressed genes regulated by RRBP1 inhibition in MB49 cells. ( B ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in MB49 cells. ( C ) KEGG analysis for differentially expressed genes found enrichment signaling pathways in tumor samples. ( D, E ) Heatmap displays the expression changes of cytokines after RRBP1 inhibition in MB49 cells and tumor tissues. ( F ) The Venn diagram illustrates the differentially expressed cytokines in both MB49 cells and tumor tissues after inhibition of RRBP1. ( G ) Representative images of IHC staining for RRBP1 and CXCL10 expression in BC samples. ( H ) The correlation between RRBP1 expression and CXCL10 expression was analyzed based on 96 patients from in-house BC cohort. Scale bar: 50 µm. ( I ) The mRNA expression of CXCL10 after genetic or pharmacological inhibition of RRBP1 in T24. ( J ) ELISA analysis of CXCL10 expression after genetic or pharmacological inhibition of RRBP1 in T24. ( K ) Distribution of RRBP1-binding peaks across CXCL10 by integrative genomics Viewer. ( L, M ) RIP analyses of MB49 cells or T24 cells were performed with an anti-RRBP1 antibody followed by qPCR analyses with primer against CXCL10 mRNA. ( N, O ) Knockdown of ENO1 to detect the CXCL10 mRNA expression levels in MB49 cells or T24 cells that were treated with actinomycin D for the indicated time. Data are represented as mean means±SD. Statistical analysis was performed using unpaired two-tailed t-test ( I, J, L, M, N, O ) or Spearman correlation analysis ( H ). The data presented represent one or three independent experiments. *p<0.05, ***p<0.001. BC, bladder cancer; mRNA, messenger RNA; qPCR, quantitative PCR; RRB1, ribosomal-binding protein 1; IHC, immunohistochemistry; KEGG, Kyoto Encyclopedia of Genes and Genomes.

    Article Snippet: After blocking with 5% non-fat milk, membranes were incubated overnight at 4°C with the following primary antibodies: anti-RRBP1 (Proteintech, 22015–1-AP, dilution 1:1000), anti-H3K36me3 (Proteintech, 61022, dilution 1:1000) and anti-GAPDH (Proteintech, 60004–1-Ig, dilution 1:2000).

    Techniques: Inhibition, Protein-Protein interactions, Expressing, Immunohistochemistry, Enzyme-linked Immunosorbent Assay, Binding Assay, Knockdown, Two Tailed Test, Real-time Polymerase Chain Reaction