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anti bap1  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology anti bap1
    Anti Bap1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 447 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+bap1/BAP1+Antibody/pmc12962116-2-0-4
    Average 96 stars, based on 447 article reviews
    anti bap1 - by Bioz Stars, 2026-09
    96/100 stars

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    other:

    Article Title: Restoration of BAP1 activity via base editing suppresses anchorage-independent survival in kidney cancer.
    Article Snippet: 19 The following primary antibodies were used in this study: anti-BAP1 (mouse IgG, 20 sc-28383; rabbit IgG, sc-28236), anti-PARP1 (sc-8007), and anti-β-actin (sc-8432) from 21 Santa Cruz Biotechnology; anti-γ-H2AX (06-636) and anti-H2A (07-146) from Millipore; 22 anti-GAPDH (LF-PA0212) from AbFrontier; anti-cyclobutane pyrimidine dimers (CPD; 23 CAC-NM-DND-001) from Cosmo Bio; and anti-H2A (12349), anti-β-catenin (9582), anti-N-24 AR TIC LE IN PR ES S cadherin (13116), anti-vimentin (5741), and anti-Cas9 (19526) from Cell Signaling 1 Technology.

    Article Title: Circular RNA hsa_Circ_0007552 inhibits lung adenocarcinoma proliferation, migration and invasion via the miR-7974/BAP1 axis
    Article Snippet: The antibodies were anti-BAP1 (Santa Cruz Biotechnology, USA, 1:500), anti-β-actin (Cell Signaling Technology, USA, 1:1000) and Goat Anti-Mouse IgG (Santa Cruz Biotechnology, USA, 1:3000).

    Article Title: ULK1-dependent phosphorylation of OGT instructs the tumorigenicity of O-GlcNAcylation.
    Article Snippet: 1Beijing Key Laboratory of DNA Damage Response and College of Life Sciences, Capital Normal University, Beijing 100048, China 2Department of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen 518036, China 3College of Life Sciences, Hebei University, Baoding 071002 China 4Department of Medical Oncology, Affiliated Hospital of Hebei University, Hebei Key Laboratory of Cancer Radiotherapy and Chemotherapy, Baoding 071000, China 5National Institute of Biological Sciences, Beijing 102206, China 6State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China 7College of Life Sciences, Mudanjiang Medical University, Mudanjiang 157011, China 8Key Laboratory of Glycoconjugate Research Ministry of Health, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China

    Article Title: Functional characterization of BAP1 mutations in genome edited cholangiocarcinoma organoids: Role in cell death and drug responses
    Article Snippet: Anti-BAP1 (mouse monoclonal) , Santa Cruz Biotechnology , Cat# sc-28383; RRID: AB_626723.

    Article Title: Restoration of BAP1 activity via base editing suppresses anchorage-independent survival in kidney cancer
    Article Snippet: The following primary antibodies were used in this study: anti-BAP1 (mouse IgG, sc-28383; rabbit IgG, sc-28236), anti-PARP1 (sc-8007), and anti-β-actin (sc-8432) from Santa Cruz Biotechnology; anti-γ-H2AX (06–636) and anti-H2A (07–146) from Millipore; anti-GAPDH (LF-PA0212) from AbFrontier; anti-cyclobutane pyrimidine dimers (CPD; CAC-NM-DND-001) from Cosmo Bio; and anti-H2A (12349), anti-β-catenin (9582), anti-N-cadherin (13116), anti-vimentin (5741), and anti-Cas9 (19526) from Cell Signaling Technology.

    Western Blot:

    Article Title: Functional analysis of O-GlcNAcylation by networking of OGT interactors and substrates.
    Article Snippet: .. For western blotting, the following primary antibodies were used at 1:1,000 dilution unless otherwise specified: anti-OGT (Proteintech, 11576-2-AP), anti-HA (C29F4), anti-Nup62 (BD Biosciences, 610498), anti-HCFC1 (Bethyl Laboratories, A301-399A-M), anti-SET1A (61702S), anti-RBBP5 (13171S), anti-BAP1 (rabbit, Bethyl Laboratories, A302-243A-M), anti-WDR5 (13105S), anti-FoxK1 (Bethyl Laboratories, A301-728A-M), anti-FoxK2 (12008S), anti-liprin-α1 (Proteintech, 14175-1-AP), anti-BAP1 (mouse, Santa Cruz Biotechnology, sc-28383), anti-O-GlcNAc (RL-2, Abcam, ab2739, 1:500) or anti-α-tubulin (MilliporeSigma, T9026, 1:3,000 or Thermo Fisher Scientific, 62204, 1:1,000). ..

    Article Title: VCP Promotes Cholangiocarcinoma Development by Mediating BAP1 Ubiquitination‐Dependent Degradation
    Article Snippet: .. Primary antibodies used for immunoblotting were as follows: anti‐BAP1 (#sc‐48386) was purchased from Santa Cruz Biotechnology (California, USA); anti‐VCP (#ET1703‐56), anti‐Caspase‐3 (#ET1602‐39), anti‐Cleaved Caspase‐3 (#ET1602‐47) and anti‐Cleaved PARP (#ET1608‐10) were from HUABIO (Hangzhou, China); anti‐PARP (#9542) was obtained from Cell Signaling Technology (Danvers, MA, USA). .. Anti‐Myc (#db457), anti‐GAPDH (#db106) and anti‐HA (#db2603) antibodies were purchased from Diagbio (Hangzhou, China).

    Marker:

    Article Title: Comprehensive molecular analysis of uveal melanoma identifies targets in tumor-intrinsic and tumor-extrinsic pathways
    Article Snippet: .. Primary antibodies used were: anti-TNFRSF14 (clone OTI7F1; OriGene Technologies; catalog # TA813628S), pan-leukocyte marker anti-CD45 (clone EP322Y; Abcam; catalog # ab40763), and anti-BAP1 (clone C-4; Santa Cruz Biotechnology; catalog # sc-28383). .. RNAScope Multiplex Fluorescent Reagent Kit v2 (Advanced Cell Diagnostics Bio-Techne; CA, USA) was used according to the manufacturer’s protocol for RNA detection.



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    (A) Frequency of <t>BAP1</t> genetic alterations in tumors from the BAP1 cancer predisposition syndrome and in pan-cancer cohorts of metastatic tumors. Patient cohorts were retrieved from QIMR Oncotarget 2016 and TCGA Firehose Legacy (UM), TCGA PanCancer Atlas (mesothelioma and kidney renal clear cell carcinoma), MSK Hepatology 2021 (intrahepatic cholangiocarcinoma), and MSK Cell 2021 (pan-cancer) datasets via the cBioPortal platform. Data are shown as bar plots. (B, C) Kaplan–Meier survival curves for overall survival (B) and disease-free survival (C) in UM patients with BAP1 wild-type (green) or BAP1-mutated (red) tumors. P-values are indicated. Data were retrieved from QIMR Oncotarget 2016 and TCGA Firehose Legacy. (D, E) Violin plots showing tumor basal diameter, tumor thickness (D), aneuploidy score, fraction of genome altered and microsatellite instability (MSI) score (E) in BAP1 wild-type versus BAP1-mutated UM patients. Orange line: median. **p < 0 . 01, *p < 0 . 05, ns: not significant . P-values were calculated using an unpaired t-test. (F) Western blot analysis of BAP1 silenced MP41 cells. (G) Western blot analysis of γH2AX in MP41 cells following BAP1 silencing. MP41 cells were treated with bleomycin (50 µg/ml, 24 h) and collected at the indicated recovery time points. (H, I) Representative immunofluorescence images of pan-nuclear γH2AX+ MP41 cells (red) at the indicated recovery time points after bleomycin treatment upon BAP1 silencing. DAPI stains DNA (blue) (H). Violin plot quantifying the percentage of pan-nuclear γH2AX+ cells per field across 3 independent experiments (I). Each dot represents a field. Red line: median. Scale bar: 10 µm. ***p < 0 . 001, **p < 0 . 01, *p < 0 . 05, ns: not significant . P-values were determined by one-way ANOVA with Tukey’s correction.
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    (A) Frequency of <t>BAP1</t> genetic alterations in tumors from the BAP1 cancer predisposition syndrome and in pan-cancer cohorts of metastatic tumors. Patient cohorts were retrieved from QIMR Oncotarget 2016 and TCGA Firehose Legacy (UM), TCGA PanCancer Atlas (mesothelioma and kidney renal clear cell carcinoma), MSK Hepatology 2021 (intrahepatic cholangiocarcinoma), and MSK Cell 2021 (pan-cancer) datasets via the cBioPortal platform. Data are shown as bar plots. (B, C) Kaplan–Meier survival curves for overall survival (B) and disease-free survival (C) in UM patients with BAP1 wild-type (green) or BAP1-mutated (red) tumors. P-values are indicated. Data were retrieved from QIMR Oncotarget 2016 and TCGA Firehose Legacy. (D, E) Violin plots showing tumor basal diameter, tumor thickness (D), aneuploidy score, fraction of genome altered and microsatellite instability (MSI) score (E) in BAP1 wild-type versus BAP1-mutated UM patients. Orange line: median. **p < 0 . 01, *p < 0 . 05, ns: not significant . P-values were calculated using an unpaired t-test. (F) Western blot analysis of BAP1 silenced MP41 cells. (G) Western blot analysis of γH2AX in MP41 cells following BAP1 silencing. MP41 cells were treated with bleomycin (50 µg/ml, 24 h) and collected at the indicated recovery time points. (H, I) Representative immunofluorescence images of pan-nuclear γH2AX+ MP41 cells (red) at the indicated recovery time points after bleomycin treatment upon BAP1 silencing. DAPI stains DNA (blue) (H). Violin plot quantifying the percentage of pan-nuclear γH2AX+ cells per field across 3 independent experiments (I). Each dot represents a field. Red line: median. Scale bar: 10 µm. ***p < 0 . 001, **p < 0 . 01, *p < 0 . 05, ns: not significant . P-values were determined by one-way ANOVA with Tukey’s correction.
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    (A) Frequency of <t>BAP1</t> genetic alterations in tumors from the BAP1 cancer predisposition syndrome and in pan-cancer cohorts of metastatic tumors. Patient cohorts were retrieved from QIMR Oncotarget 2016 and TCGA Firehose Legacy (UM), TCGA PanCancer Atlas (mesothelioma and kidney renal clear cell carcinoma), MSK Hepatology 2021 (intrahepatic cholangiocarcinoma), and MSK Cell 2021 (pan-cancer) datasets via the cBioPortal platform. Data are shown as bar plots. (B, C) Kaplan–Meier survival curves for overall survival (B) and disease-free survival (C) in UM patients with BAP1 wild-type (green) or BAP1-mutated (red) tumors. P-values are indicated. Data were retrieved from QIMR Oncotarget 2016 and TCGA Firehose Legacy. (D, E) Violin plots showing tumor basal diameter, tumor thickness (D), aneuploidy score, fraction of genome altered and microsatellite instability (MSI) score (E) in BAP1 wild-type versus BAP1-mutated UM patients. Orange line: median. **p < 0 . 01, *p < 0 . 05, ns: not significant . P-values were calculated using an unpaired t-test. (F) Western blot analysis of BAP1 silenced MP41 cells. (G) Western blot analysis of γH2AX in MP41 cells following BAP1 silencing. MP41 cells were treated with bleomycin (50 µg/ml, 24 h) and collected at the indicated recovery time points. (H, I) Representative immunofluorescence images of pan-nuclear γH2AX+ MP41 cells (red) at the indicated recovery time points after bleomycin treatment upon BAP1 silencing. DAPI stains DNA (blue) (H). Violin plot quantifying the percentage of pan-nuclear γH2AX+ cells per field across 3 independent experiments (I). Each dot represents a field. Red line: median. Scale bar: 10 µm. ***p < 0 . 001, **p < 0 . 01, *p < 0 . 05, ns: not significant . P-values were determined by one-way ANOVA with Tukey’s correction.
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    Image Search Results


    (A) Frequency of BAP1 genetic alterations in tumors from the BAP1 cancer predisposition syndrome and in pan-cancer cohorts of metastatic tumors. Patient cohorts were retrieved from QIMR Oncotarget 2016 and TCGA Firehose Legacy (UM), TCGA PanCancer Atlas (mesothelioma and kidney renal clear cell carcinoma), MSK Hepatology 2021 (intrahepatic cholangiocarcinoma), and MSK Cell 2021 (pan-cancer) datasets via the cBioPortal platform. Data are shown as bar plots. (B, C) Kaplan–Meier survival curves for overall survival (B) and disease-free survival (C) in UM patients with BAP1 wild-type (green) or BAP1-mutated (red) tumors. P-values are indicated. Data were retrieved from QIMR Oncotarget 2016 and TCGA Firehose Legacy. (D, E) Violin plots showing tumor basal diameter, tumor thickness (D), aneuploidy score, fraction of genome altered and microsatellite instability (MSI) score (E) in BAP1 wild-type versus BAP1-mutated UM patients. Orange line: median. **p < 0 . 01, *p < 0 . 05, ns: not significant . P-values were calculated using an unpaired t-test. (F) Western blot analysis of BAP1 silenced MP41 cells. (G) Western blot analysis of γH2AX in MP41 cells following BAP1 silencing. MP41 cells were treated with bleomycin (50 µg/ml, 24 h) and collected at the indicated recovery time points. (H, I) Representative immunofluorescence images of pan-nuclear γH2AX+ MP41 cells (red) at the indicated recovery time points after bleomycin treatment upon BAP1 silencing. DAPI stains DNA (blue) (H). Violin plot quantifying the percentage of pan-nuclear γH2AX+ cells per field across 3 independent experiments (I). Each dot represents a field. Red line: median. Scale bar: 10 µm. ***p < 0 . 001, **p < 0 . 01, *p < 0 . 05, ns: not significant . P-values were determined by one-way ANOVA with Tukey’s correction.

    Journal: bioRxiv

    Article Title: BAP1 loss impairs Non-Homologous End Joining DNA repair promoting genomic instability

    doi: 10.64898/2026.02.17.706330

    Figure Lengend Snippet: (A) Frequency of BAP1 genetic alterations in tumors from the BAP1 cancer predisposition syndrome and in pan-cancer cohorts of metastatic tumors. Patient cohorts were retrieved from QIMR Oncotarget 2016 and TCGA Firehose Legacy (UM), TCGA PanCancer Atlas (mesothelioma and kidney renal clear cell carcinoma), MSK Hepatology 2021 (intrahepatic cholangiocarcinoma), and MSK Cell 2021 (pan-cancer) datasets via the cBioPortal platform. Data are shown as bar plots. (B, C) Kaplan–Meier survival curves for overall survival (B) and disease-free survival (C) in UM patients with BAP1 wild-type (green) or BAP1-mutated (red) tumors. P-values are indicated. Data were retrieved from QIMR Oncotarget 2016 and TCGA Firehose Legacy. (D, E) Violin plots showing tumor basal diameter, tumor thickness (D), aneuploidy score, fraction of genome altered and microsatellite instability (MSI) score (E) in BAP1 wild-type versus BAP1-mutated UM patients. Orange line: median. **p < 0 . 01, *p < 0 . 05, ns: not significant . P-values were calculated using an unpaired t-test. (F) Western blot analysis of BAP1 silenced MP41 cells. (G) Western blot analysis of γH2AX in MP41 cells following BAP1 silencing. MP41 cells were treated with bleomycin (50 µg/ml, 24 h) and collected at the indicated recovery time points. (H, I) Representative immunofluorescence images of pan-nuclear γH2AX+ MP41 cells (red) at the indicated recovery time points after bleomycin treatment upon BAP1 silencing. DAPI stains DNA (blue) (H). Violin plot quantifying the percentage of pan-nuclear γH2AX+ cells per field across 3 independent experiments (I). Each dot represents a field. Red line: median. Scale bar: 10 µm. ***p < 0 . 001, **p < 0 . 01, *p < 0 . 05, ns: not significant . P-values were determined by one-way ANOVA with Tukey’s correction.

    Article Snippet: The following primary antibodies were incubated overnight at 4°C: rabbit BAP1 (D7W70) mAB (Cell Signaling Technology, 13271S), mouse Anti-β-Actin (Sigma Aldrich, A1978-200UL), mouse BRCA1 (D-9) monoclonal IgG (Santa Cruz Biotechnology, sc-6954), mouse monoclonal anti-GAPDH, clone GAPDH-71.1 (Sigma Aldrich, G8795-200UL), mouse Anti-phospho-Histone H2A.X (Ser139), clone JBW301 (Merck/Sigma, 05-636-I), rabbit H3 (D1H2) mAb (Cell Signaling, # 4499), Ubiquityl-Histone H2A (Lys119) (D27C4) XP® Rabbit mAb (Cell Signaling, #8240) and anti-Histone H2A (Abcam, ab18255).

    Techniques: Western Blot, Immunofluorescence

    (A) Western blot analysis of H2AK119ub levels upon BAP1 depletion in G1 cells. MP41 were irradiated (5 Gy) at 6 hours from Nocodazole release and collected 3 hours post IR (B, C) Scatter dot plots quantifying RPA foci (green in C) during recovery from bleomycin treatment in MP41 cells depleted of BAP1. Representative immunofluorescence images are shown in B. DAPI stains DNA. Scale bar: 10 µm. Red line: mean. ****p < 0.0001, **p < 0.01, ns: not significant. P-values by one-way ANOVA with Tukey’s correction (D–F) Scatter dot plots quantifying RPA foci in Cyclin A2+ cells (panel D), Cyclin A2– cells (G1 phase, panel E) in MP41 cells depleted of BAP1. Representative immunofluorescence images are shown in F. Red line: mean. *p < 0.05, **p < 0.01, ns: not significant. P-values by one-way ANOVA with Tukey’s correction.

    Journal: bioRxiv

    Article Title: BAP1 loss impairs Non-Homologous End Joining DNA repair promoting genomic instability

    doi: 10.64898/2026.02.17.706330

    Figure Lengend Snippet: (A) Western blot analysis of H2AK119ub levels upon BAP1 depletion in G1 cells. MP41 were irradiated (5 Gy) at 6 hours from Nocodazole release and collected 3 hours post IR (B, C) Scatter dot plots quantifying RPA foci (green in C) during recovery from bleomycin treatment in MP41 cells depleted of BAP1. Representative immunofluorescence images are shown in B. DAPI stains DNA. Scale bar: 10 µm. Red line: mean. ****p < 0.0001, **p < 0.01, ns: not significant. P-values by one-way ANOVA with Tukey’s correction (D–F) Scatter dot plots quantifying RPA foci in Cyclin A2+ cells (panel D), Cyclin A2– cells (G1 phase, panel E) in MP41 cells depleted of BAP1. Representative immunofluorescence images are shown in F. Red line: mean. *p < 0.05, **p < 0.01, ns: not significant. P-values by one-way ANOVA with Tukey’s correction.

    Article Snippet: The following primary antibodies were incubated overnight at 4°C: rabbit BAP1 (D7W70) mAB (Cell Signaling Technology, 13271S), mouse Anti-β-Actin (Sigma Aldrich, A1978-200UL), mouse BRCA1 (D-9) monoclonal IgG (Santa Cruz Biotechnology, sc-6954), mouse monoclonal anti-GAPDH, clone GAPDH-71.1 (Sigma Aldrich, G8795-200UL), mouse Anti-phospho-Histone H2A.X (Ser139), clone JBW301 (Merck/Sigma, 05-636-I), rabbit H3 (D1H2) mAb (Cell Signaling, # 4499), Ubiquityl-Histone H2A (Lys119) (D27C4) XP® Rabbit mAb (Cell Signaling, #8240) and anti-Histone H2A (Abcam, ab18255).

    Techniques: Western Blot, Irradiation, Immunofluorescence

    (A) Representative immunofluorescence images of RPA (green) and Cyclin A2 (red) in BAP1-depleted MP41 cells ± PTC-209 treatment. DAPI stains DNA. Cells were treated with PTC-209 (0.1 µM, 48 h) prior to irradiation and collected at 3 h post-IR. Arrows mark Cyclin A2– (G1 phase) cells with RPA foci. Scale bar: 10 µm. (B, C) Scatter dot plots showing (B) the percentage of RPA+ Cyclin A2– cells and (C) the number of RPA foci per Cyclin A2– cell at 3 h post-IR. Red line: mean. ****p < 0.0001, ***p < 0.001, **p < 0.01, ns: not significant. P-values by one-way ANOVA with Tukey’s correction. (D) Representative immunofluorescence images of 53BP1 (green) in BAP1-depleted MP41 cells ± PTC-209 treatment at 1 and 3 h post-IR. DAPI stains DNA. Scale bar: 10 µm. (E) Scatter dot plot quantifying 53BP1 foci per cell. Red line: median. ****p < 0.0001, **p < 0.01, ns: not significant. P-values by one-way ANOVA with Tukey’s correction. (F) Schematic model. In BAP1-proficient cells, BAP1 deubiquitylates H2AK119ub deposited by PRC1, permitting 53BP1 recruitment and NHEJ execution in G1. In BAP1-depleted cells, H2AK119ub accumulates, blocking 53BP1 loading, and driving aberrant DNA end resection with RPA recruitment in G1, where HR is not available.

    Journal: bioRxiv

    Article Title: BAP1 loss impairs Non-Homologous End Joining DNA repair promoting genomic instability

    doi: 10.64898/2026.02.17.706330

    Figure Lengend Snippet: (A) Representative immunofluorescence images of RPA (green) and Cyclin A2 (red) in BAP1-depleted MP41 cells ± PTC-209 treatment. DAPI stains DNA. Cells were treated with PTC-209 (0.1 µM, 48 h) prior to irradiation and collected at 3 h post-IR. Arrows mark Cyclin A2– (G1 phase) cells with RPA foci. Scale bar: 10 µm. (B, C) Scatter dot plots showing (B) the percentage of RPA+ Cyclin A2– cells and (C) the number of RPA foci per Cyclin A2– cell at 3 h post-IR. Red line: mean. ****p < 0.0001, ***p < 0.001, **p < 0.01, ns: not significant. P-values by one-way ANOVA with Tukey’s correction. (D) Representative immunofluorescence images of 53BP1 (green) in BAP1-depleted MP41 cells ± PTC-209 treatment at 1 and 3 h post-IR. DAPI stains DNA. Scale bar: 10 µm. (E) Scatter dot plot quantifying 53BP1 foci per cell. Red line: median. ****p < 0.0001, **p < 0.01, ns: not significant. P-values by one-way ANOVA with Tukey’s correction. (F) Schematic model. In BAP1-proficient cells, BAP1 deubiquitylates H2AK119ub deposited by PRC1, permitting 53BP1 recruitment and NHEJ execution in G1. In BAP1-depleted cells, H2AK119ub accumulates, blocking 53BP1 loading, and driving aberrant DNA end resection with RPA recruitment in G1, where HR is not available.

    Article Snippet: The following primary antibodies were incubated overnight at 4°C: rabbit BAP1 (D7W70) mAB (Cell Signaling Technology, 13271S), mouse Anti-β-Actin (Sigma Aldrich, A1978-200UL), mouse BRCA1 (D-9) monoclonal IgG (Santa Cruz Biotechnology, sc-6954), mouse monoclonal anti-GAPDH, clone GAPDH-71.1 (Sigma Aldrich, G8795-200UL), mouse Anti-phospho-Histone H2A.X (Ser139), clone JBW301 (Merck/Sigma, 05-636-I), rabbit H3 (D1H2) mAb (Cell Signaling, # 4499), Ubiquityl-Histone H2A (Lys119) (D27C4) XP® Rabbit mAb (Cell Signaling, #8240) and anti-Histone H2A (Abcam, ab18255).

    Techniques: Immunofluorescence, Irradiation, Blocking Assay