pbrm1 antibody (Fortis Life Sciences)
Fortis Life Sciences is a verified supplier 
Fortis Life Sciences manufactures this product 
94
Structured Review
Fortis Life Sciences
pbrm1 antibody
Pbrm1 Antibody, supplied by Fortis Life Sciences, used in various techniques. Bioz Stars score: 94/100, based on 118 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tissue+microarray+based+immunohistochemistry+analysis/PBRM1+Antibody/pmc07195420-289-0-5
Average 94 stars, based on 118 article reviews
Pbrm1 Antibody, supplied by Fortis Life Sciences, used in various techniques. Bioz Stars score: 94/100, based on 118 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tissue+microarray+based+immunohistochemistry+analysis/PBRM1+Antibody/pmc07195420-289-0-5
Average 94 stars, based on 118 article reviews
pbrm1 antibody - by Bioz Stars,
2026-11
94/100 stars
Images
1) Product Images from "PBRM1 loss defines a nonimmunogenic tumor phenotype associated with checkpoint inhibitor resistance in renal carcinoma"
Article Title: PBRM1 loss defines a nonimmunogenic tumor phenotype associated with checkpoint inhibitor resistance in renal carcinoma
Journal: Nature Communications
doi: 10.1038/s41467-020-15959-6
Figure Legend Snippet: a Pbrm1 knockout validation in Renca cells at protein levels by western blot, and b at mRNA levels by real-time PCR. Renca cell were treated with or without 1 ng/ml IFNγ for 8 h. c IFNγ-induced JAK-STAT1 expression and phosphorylation in Renca cells. Control KO or Pbrm1 KO (clone #18) Renca cells were treated with 1 ng/ml IFNγ for 2 or 8 h. Cell lysates were analyzed by immunoblot using antibodies against PBRM1, STAT1, P-STA1 Y701, P-STAT1 S727, JAK2, P-JAK2 Y1007/1008, JAK1, P-JAK1 Y1034/1035, IRF1. β-actin was used an internal control. d IFNγ-induced gene expression in Renca cells. Control KO or Pbrm1 KO (clone #18) Renca cells were treated with 1 ng ml IFNγ for 8 h. mRNA expression of Stat1 , Cxcl9 , Irf1 , and Icam1 were detected by real-time PCR. Gapdh was used as internal control. e IFNγ-induced CXCL9 secretion. Renca cells were cultured in serum-free medium and treated with 1 ng/ml IFNγ for 4 or 10 h. The concentration of CXCL9 was analyzed using Quantikine® ELISA kit. f IFNγ-induced JAK-STAT1 expression and phosphorylation in 786-O cells. Control knockdown (Con KD) or PBRM1 knockdown ( PBRM1 KD) 786-O cells were treated with or without 10 ng/ml IFNγ for 2 h. Cell lysates were analyzed by immunoblot using antibodies against PBRM1, STAT1, P-STA1 Y701, JAK2, P-JAK2 Y1007/1008, and IRF1. β-actin was used an internal control. g IFNγ-induced gene expression in 786-O cells. 786-O cells were cultured in DMEM with 10% FBS, and treated with 10 ng/ml IFNγ for 8 h. mRNA expression of STAT1 , CXCL9 , and IRF1 were detected by real-time PCR. GAPDH was used as internal control. Unpaired t -test was performed with GraphPad Prism 7.03. * P < 0.05 and ** P < 0.001, compared with control knockout or knockdown cells. All data are representative of three independent experiments. Data in the bar graphs represent mean ± S.D., n = 3. Source data are provided as a Source Data file.
Techniques Used: Knock-Out, Western Blot, Real-time Polymerase Chain Reaction, Expressing, Cell Culture, Concentration Assay, Enzyme-linked Immunosorbent Assay
Figure Legend Snippet: a BRG1 and STAT1 binding to Cxcl9 and Cxcl10 promoter in Renca cells. b BRG1 and SP1 binding to Ifngr2 promoter. Chromatin immunoprecipitation (ChIP) with BRG1, STAT1 or SP1 antibody as indicated in figures was performed using SimpleChIP® Plus Enzymatic Chromatin IP Kit. Isotype IgG was used as negative control. Immunoprecipitated DNA was amplified and quantified by real-time PCR. Protein relative occupancy on promoter was expressed as a percent of the total input chromatin. Con KO or Pbrm1 KO Renca cells were treated with 1 ng/ml IFNγ for 2 h for IFNγ-induced STAT1 binding to Cxcl9 or Cxcl10 promoter. c IFNγ receptor subunits, Ifngr1 and Ifngr2 , mRNA expression detected by real-time PCR. Gapdh was used as internal control. d IFNγ receptor subunits, IFNGR1 and IFNGR2, protein expression was detected by western blot. β-actin was used an internal control. e IFNGR2 membrane expression was detected by flow cytometry. Unpaired t -test was performed with GraphPad Prism 7.03. * P < 0.05 and ** P < 0.001, compared with control knockout cells. Data in the bar graphs represent mean ± S.D. Source data are provided as a Source Data file.
Techniques Used: Binding Assay, Chromatin Immunoprecipitation, Negative Control, Immunoprecipitation, Amplification, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Flow Cytometry, Knock-Out
Figure Legend Snippet: a The confidence interval plots represented the differences in these genes between the two groups ( Pbrm1 KO minus Pbrm1 WT). The x -axis is the difference in group means of Pbrm1 knockout group minus Pbrm1 wild-type group, so negative values correspond to genes downregulated in the Pbrm1 knockout group. The lines depicted 95% confidence intervals, and genes with a significant difference between the groups (adjusted P -value <0.05) were marked in orange. The P -values were obtained from a two-sample t-test on the log2-transformed values, and the resulting P -values were adjusted for multiple comparisons using the Benjamini–Hochberg method across the gene set. b mRNA expressions of Ifng , Cxcl9 , Cxcl10 , and Pdcd1 and c the mRNA expression of Pbrm1 , Ifngr1 , Ifngr2 , and Cd274 were detected by real-time PCR. Each dot represents the mean value of triplicated tumor samples. Unpaired t -test was performed with GraphPad Prism 7.03. d The coordinated differences of the genes as listed in ( a ) across the two groups assessed by gene set enrichment analysis (GSEA). e T cell infiltration and quantification. Murine Renca tumor microarrays, with triplicate formalin-fixed tissue cores for each case, were immunohistochemically stained with antibodies against CD3, CD8, CD4, PD-1, and P-STAT1 Y701. The percentages of positively stained cells were analyzed using inForm software. Unpaired t-test was performed with GraphPad Prism 7.03. Scale bar, 100 µm. f Multiplex Opal Immunofluorescence staining. The slides were stained with primary antibodies against CD8 and PD-1, corresponding HRP conjugated secondary antibodies, and subsequently TSA dyes to generate Opal signal (CD8, 520 nm; PD-1, 570 nm). PD-1 Opal signals are artificially colored as red. Scale bar, 50 µm. g Immunomodulatory gene expression signature score in pre-malignant murine kidneys following loss of Vhl alone ( Vhl −/− ), or Vhl in combination with Pbrm1 ( Vhl −/− Pbrm1 −/− ). Student t -test. h Gene expression-based inference of total T cell and CD8 T-cell infiltrates in pre-malignant murine kidneys following loss of Vhl alone, or Vhl in combination with Pbrm1 . Student t -test. Data in the graphs represent mean ± S.D. Source data are provided as a Source Data file.
Techniques Used: Knock-Out, Transformation Assay, Expressing, Real-time Polymerase Chain Reaction, Staining, Software, Multiplex Assay, Immunofluorescence
Figure Legend Snippet: a The confidence interval plots represented the differences in immunomodulatory genes between the two groups (mutant PBRM1 minus wild-type PBRM1 ) in TCGA KIRC dataset. MUT, mutant PBRM1 ; WT, wild-type PBRM1 . The lines depicted 95% confidence intervals, and genes with a significant difference between the groups (adjusted P -value <0.05) were marked in orange. The P -values were obtained from a two-sample t -test on the log2-transformed values, and the resulting P -values were adjusted for multiple comparisons using the Benjamini–Hochberg method across the gene set. b Comparison of gene expression in tumors with mutant PBRM1 (MUT) versus wild-type PBRM1 (WT) by GSEA using the immunomodulatory genes as listed in ( a ) and other predefined immune-related gene sets in the TCGA, IMmotion150 and ICGC patient cohorts. c Comparison of CD8 infiltrates as assessed by immunohistochemistry for CD8 in the IMmotion150 patient cohort. Rank-sum test. d CD8 immunostaining levels positively correlated with gene expression-based inference. Spearman correlation and associated P -value inset. e Gene expression-based inference of CD8 T cell infiltrates in patients stratified by PBRM1 mutation status. Rank-sum test. f Comparison of immune cell PD-L1 expression in patients from the IMmotion150 cohort stratified by PBRM1 mutation status. Cochran–Armitage test for trend. g Treatment naive RCC tumor microarray from 20 untreated RCC patients, including 15 samples with wild-type PBRM1 and 5 with PBRM1 mutations, were immunohistochemically stained with antibodies against CD3, CD45RO, CD8, and CD4. Each tumor was triplicated, and the n values indicate the number of the intact cores. The percentages of positively stained cells were analyzed using inForm software. Non-parametric Mann–Whitney test was performed with GraphPad Prism 7.03. Scale bar, 100 µm. h Multiplex Opal immunofluorescence staining. The slides were stained with primary antibodies against CD8 and PD-1, corresponding HRP conjugated secondary antibodies, and subsequently TSA dyes to generate Opal signal (CD8, 520 nm; PD-1, 620 nm). Scale bar, 50 µm. Data in the graphs represent mean ± S.D. Source data are provided as a Source Data file.
Techniques Used: Mutagenesis, Transformation Assay, Expressing, Immunohistochemistry, Immunostaining, Microarray, Staining, Software, MANN-WHITNEY, Multiplex Assay, Immunofluorescence
Figure Legend Snippet: a Correlogram between the expression of immunomodulatory and angiogenic genes IMmotion 150 cohort (top line of each square), TCGA cohort (middle line of each square) and ICGC cohort (bottom line of each square). b Patients with mutant PBRM1 demonstrated increased CD31 immunostaining levels in the IMmotion150 cohort. Rank-sum test. c CD31 immunostaining levels positively correlated with angiogenesis expression score. Spearman correlation and associated P -value inset ( N = 119). d PBRM1 mutated tumors were associated with increased angiogenesis score in 3 indicated patient cohorts. Rank-sum test. e Pbrm1 knockout was associated with increased angiogenesis score in pre-malignant murine kidneys. Student t -test. f Pbrm1 knockout Renca tumors demonstrated increased CD31 immunostaining levels. Student t -test. Data in the bar graphs represent mean ± S.D. Source data are provided as a Source Data file.
Techniques Used: Expressing, Mutagenesis, Immunostaining, Knock-Out
Figure Legend Snippet: a Early treatment with anti-PD-1 blockade. PD-1 antibodies were administrated at day 3, day 6, and day 9 after tumor inoculation. First dose was 400 µg/mouse, and the following two doses were 200 µg/mouse. b Delayed treatment with anti-PD-1 blockade. Anti-PD-1 antibody (200 µg/mouse) was administrated every third day once the tumors reached 100-200 mm 3 . Treatment schemas, In vivo tumor growth rates and survival rates of mice are shown. Two-way ANOVA and Log-rank (Mantel-Cox) analyses were performed with GraphPad Prism 7.03. Data in the graphs are means ± SEM. UnTX, untreated control. ns, P > 0.05, * P < 0.05, and ** P < 0.001. c Patient response in the IMmotion150 cohort following treatment with either atezolizumab (Atezo) or atezolizumab in combination with bevacizumab (Atezo + Bev). Mono, PBRM1 mutation only, Dual, PBRM1 mutation in combination with a BAP1 or SETD2 mutation; WT, wild type; CR, complete response; PR, partial response; SD, stable disease; PD, progressive disease. Cochran–Mantel–Haenszel test. d Comparison of patient response rate, defined as either a complete or partial response, in the IMmotion150 cohort. Cochran–Mantel–Haenszel test. e Overall survival of RCC patients treated with ICB from the MSKCC IMPACT cohort stratified by PBRM1 status. Log-rank test. f Overall survival of ccRCC patients from TCGA stratified by PBRM1 mutation status. Log-rank test. g Model for PBRM1 mediated IFNγ-STAT1 signaling and tumor immune microenvironment modulating. PBRM1 ensures IFNγ-induced STAT1 activity and autonomous expression of downstream genes involved in T-cell recruitment (e.g., CXCL9 ). Infiltrating, activated T cells in turn produce more IFNγ which stimulates tumor cells to secrete immunostimulatory chemokines and cytokines, and in parallel upregulate checkpoint pathways on T cells and tumors cells. Thus, the immunogenic TME of PBRM1 proficient tumors is primed to respond to ICB. On the other hand, PBRM1 loss reduces IFNγ-STAT1 signaling and downstream T cell attracting factors, which prevents T cell infiltration and IFNγ secretion. Such a non-immunogenic TME of PBRM1 mutated tumors blunts ICB response. Source data are provided as a Source Data file.
Techniques Used: In Vivo, Mutagenesis, Activity Assay, Expressing
Related Articles
other:Article Title: PBRM1-VHL cooperation rewires lipid and iron metabolism to promote ferroptosis resistance in clear cell renal cell carcinoma Article Snippet: In-house purified pAG-MNase was used; the construct was obtained from Addgene (Watertown, MA, USA; #123461; gift from Steven Henikoff) and purified as previously described. Article Title: A single chromosome 3p break initiates clear cell renal cell carcinoma evolution Article Snippet: Z-stacks were acquired at 0.2 μm intervals (typically 11-15 sections) and deconvolved maximum intensity projections were generated using softWoRx (v7.2.1, Cytiva). Article Title: Loss of Brg1 and Pten in Pancreatic Ductal Cells Forms Intraductal Tubulopapillary Neoplasm via the YAP/TAZ Pathway Article Snippet: PBRM1 , Article Title: Pbrm1 Loss Induces a Permissive Chromatin State for Cholangiocytic Differentiation and Cholangiocarcinoma Formation Article Snippet: PBRM1 , 1:100 , Immunostaining:Article Title: BAP1 and PBRM1 Loss Is Associated with Aggressive Clinicopathological Features in Clear Cell Renal Cell Carcinoma: Prognostic Implications in a 10-Year Surgical Cohort Article Snippet: Antigen retrieval was performed using CC1 high pH buffer at 95 °C for 92 min. Signal detection was carried out using the ultraView detection system (Roche Diagnostics) with amplification (Amplification Kit, catalog no. 05266114001, Roche Diagnostics), according to the manufacturer’s protocol. .. Incubation:Article Title: BAP1 and PBRM1 Loss Is Associated with Aggressive Clinicopathological Features in Clear Cell Renal Cell Carcinoma: Prognostic Implications in a 10-Year Surgical Cohort Article Snippet: Antigen retrieval was performed using CC1 high pH buffer at 95 °C for 92 min. Signal detection was carried out using the ultraView detection system (Roche Diagnostics) with amplification (Amplification Kit, catalog no. 05266114001, Roche Diagnostics), according to the manufacturer’s protocol. .. Western Blot:Article Title: Sexually dimorphic effects of mutations in ccRCC driver genes in renal proximal tubule cells Article Snippet: Cultured cells were lysed in RIPA (Radioimmunoprecipitation assay) buffer (50 mM Tris–HCl at pH 8.0, 150 mM sodium chloride, 1% (v/v) NP-40, 0.5% (w/v) sodium deoxycholate, 0.1% (w/v) SDS (sodium dodecyl sulfate), 5 mM sodium fluoride, 1 mM sodium orthovanadate, 1mM PMSF (phenylmethylsulphonyl fluoride) and Protease Inhibitor Cocktail (1:100, Sigma Aldrich). .. Western blots were probed with the following antibodies anti-pVHL(m)(1:2000, ref. ), Article Title: MUCIN 1 confers inflammatory memory of tyrosine kinase inhibitor resistance in non-small cell lung cancer Article Snippet: .. Immunoblot analysis was performed as described using anti-MUC1-C (#MA5–11202, 1:1000 dilution; Thermo Fisher Scientific), anti-β-actin (A5441, 1:5000 dilution; Sigma-Aldrich, Burlington, MA, USA), anti-p-STAT1 (#9167, 1:1000 dilution; CST), anti-STAT1 (#9172, 1:1000 dilution; CST), anti-OAS1 (#14498, 1:1000 dilution; CST), anti-MX1 (37849, 1:1000 dilution; CST), anti-ISG15 (sc-166755, 1:250 dilution; Santa Cruz, Santa Cruz Biotechnology), |
