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mouse anti brca1 primary antibody (Santa Cruz Biotechnology)

Name: mouse anti brca1 primary antibody
Brand: Santa Cruz Biotechnology
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Santa Cruz Biotechnology mouse anti brca1 primary antibody
Correlation between RAD51-IF score and HRR gene alterations

Mouse Anti Brca1 Primary Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1009 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 96 stars, based on 1009 article reviews

mouse anti brca1 primary antibody - by Bioz Stars, 2026-03

96/100 stars

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1) Product Images from "Homologous recombination repair status in metastatic prostate cancer by next-generation sequencing and functional immunofluorescence"

Article Title: Homologous recombination repair status in metastatic prostate cancer by next-generation sequencing and functional immunofluorescence

Journal: Cell Reports Medicine

doi: 10.1016/j.xcrm.2025.101937

Figure Legend Snippet: Correlation between RAD51-IF score and HRR gene alterations

Techniques Used:

Representative cases correlating RAD51-IF score and genomic characterization Images of the RAD51 and yH2AX staining from (A) a RAD51 high sample with no HRR alterations, (B) a RAD51 low case with a BRCA2 pathogenic mutation, (C) a liver biopsy of a patient with a BRCA2 pathogenic mutation after progression to platinum-based chemotherapy that shows high percentage of cells positive for RAD51 foci; contemporaneous ctDNA analysis demonstrated BRCA2 reversion mutations. CT scan (left) of the liver lesions of the patient from baseline, response, and progression to carboplatin. Liver lesions are highlighted in yellow. Representative image of the RAD51 positivity (right) by IF and (D) prostate and liver biopsies of a patient with a monoallelic somatic BRCA1 mutation detected by NGS. The primary prostate tumor shows RAD51-negative cells, but the liver metastasis shows high RAD51 score, in parallel to BRCA1 expression by IF in this liver lesion, but not in the prostate tumor, suggesting restoration of BRCA1 expression in the metastases. Scale bar: 50 μm.

Figure Legend Snippet: Representative cases correlating RAD51-IF score and genomic characterization Images of the RAD51 and yH2AX staining from (A) a RAD51 high sample with no HRR alterations, (B) a RAD51 low case with a BRCA2 pathogenic mutation, (C) a liver biopsy of a patient with a BRCA2 pathogenic mutation after progression to platinum-based chemotherapy that shows high percentage of cells positive for RAD51 foci; contemporaneous ctDNA analysis demonstrated BRCA2 reversion mutations. CT scan (left) of the liver lesions of the patient from baseline, response, and progression to carboplatin. Liver lesions are highlighted in yellow. Representative image of the RAD51 positivity (right) by IF and (D) prostate and liver biopsies of a patient with a monoallelic somatic BRCA1 mutation detected by NGS. The primary prostate tumor shows RAD51-negative cells, but the liver metastasis shows high RAD51 score, in parallel to BRCA1 expression by IF in this liver lesion, but not in the prostate tumor, suggesting restoration of BRCA1 expression in the metastases. Scale bar: 50 μm.

Techniques Used: Staining, Mutagenesis, Computed Tomography, Expressing

Figure Legend Snippet:

Techniques Used: Recombinant, Software

Image Search Results

Journal: Cell Reports Medicine

Article Title: Homologous recombination repair status in metastatic prostate cancer by next-generation sequencing and functional immunofluorescence

doi: 10.1016/j.xcrm.2025.101937

Figure Lengend Snippet: Correlation between RAD51-IF score and HRR gene alterations

Article Snippet: The following primary antibodies were used: rabbit anti-RAD51 (Abcam ab133534, 1:1,000), mouse anti-GMN (NovoCastra NCL-L, 1:60), rabbit anti-GMN (ProteinTech 10802–1-AP, 1:400), and mouse anti-γH2AX (Millipore #05636, 1:200); additionally, BRCA1 expression was assessed in selected cases using a mouse anti-BRCA1 primary antibody (Santa Cruz Biotechnology Inc, Dallas, TX sc-6954, 1:50).

Techniques:

Journal: Cell Reports Medicine

Article Title: Homologous recombination repair status in metastatic prostate cancer by next-generation sequencing and functional immunofluorescence

doi: 10.1016/j.xcrm.2025.101937

Figure Lengend Snippet: Representative cases correlating RAD51-IF score and genomic characterization Images of the RAD51 and yH2AX staining from (A) a RAD51 high sample with no HRR alterations, (B) a RAD51 low case with a BRCA2 pathogenic mutation, (C) a liver biopsy of a patient with a BRCA2 pathogenic mutation after progression to platinum-based chemotherapy that shows high percentage of cells positive for RAD51 foci; contemporaneous ctDNA analysis demonstrated BRCA2 reversion mutations. CT scan (left) of the liver lesions of the patient from baseline, response, and progression to carboplatin. Liver lesions are highlighted in yellow. Representative image of the RAD51 positivity (right) by IF and (D) prostate and liver biopsies of a patient with a monoallelic somatic BRCA1 mutation detected by NGS. The primary prostate tumor shows RAD51-negative cells, but the liver metastasis shows high RAD51 score, in parallel to BRCA1 expression by IF in this liver lesion, but not in the prostate tumor, suggesting restoration of BRCA1 expression in the metastases. Scale bar: 50 μm.

Techniques: Staining, Mutagenesis, Computed Tomography, Expressing

Journal: Cell Reports Medicine

Article Title: Homologous recombination repair status in metastatic prostate cancer by next-generation sequencing and functional immunofluorescence

doi: 10.1016/j.xcrm.2025.101937

Figure Lengend Snippet:

Techniques: Recombinant, Software

Representative images of BRCA1 and FANCD2 staining in benign and malignant tumor tissues of patients with BC at ×200 magnification. (A) Negative control of BRCA1 in BC tissues. (B) Negative control of FANCD2 in BC tissue. Positive control of BRCA1 in (C) the nuclei and (D) cytoplasm of BC tissue. (E) Positive control of FANCD2 in the nuclei of BC tissues. (F) Positive expression of BRCA1 in the nuclei, (G) BRCA1 in the cytoplasm and (H) FANCD2 in the nuclei of BC tissues. Positive expression of (I) BRCA1 in the nuclei, (J) BRCA1 in the cytoplasm and (K) FANCD2 in the nuclei of the tissues adjacent to the carcinoma. Positive expression of (L) BRCA1 in the nuclei, (M) BRCA1 in the cytoplasm and (N) FANCD2 in the nuclei of benign tissues. (O) Negative expression of FANCD2 in benign tissue. BC, breast cancer; BRCA1, breast cancer type 1 susceptibility protein; FANCD2 Fanconi anemia group D2 protein.

Journal: Oncology Letters

Article Title: Expression and prognostic significance of Fanconi anemia group D2 protein and breast cancer type 1 susceptibility protein in familial and sporadic breast cancer

doi: 10.3892/ol.2019.10046

Figure Lengend Snippet: Representative images of BRCA1 and FANCD2 staining in benign and malignant tumor tissues of patients with BC at ×200 magnification. (A) Negative control of BRCA1 in BC tissues. (B) Negative control of FANCD2 in BC tissue. Positive control of BRCA1 in (C) the nuclei and (D) cytoplasm of BC tissue. (E) Positive control of FANCD2 in the nuclei of BC tissues. (F) Positive expression of BRCA1 in the nuclei, (G) BRCA1 in the cytoplasm and (H) FANCD2 in the nuclei of BC tissues. Positive expression of (I) BRCA1 in the nuclei, (J) BRCA1 in the cytoplasm and (K) FANCD2 in the nuclei of the tissues adjacent to the carcinoma. Positive expression of (L) BRCA1 in the nuclei, (M) BRCA1 in the cytoplasm and (N) FANCD2 in the nuclei of benign tissues. (O) Negative expression of FANCD2 in benign tissue. BC, breast cancer; BRCA1, breast cancer type 1 susceptibility protein; FANCD2 Fanconi anemia group D2 protein.

Article Snippet: Tissues were blocked with 1% bovine serum albumin (Reagent A, KIT-9710 UltraSensitiveTM SP (Mouse/Rabbit) IHC Kit, MXB Biotechnology) at room temperature to avoid non-specific binding, and labeled with the mouse anti-human primary antibodies against BRCA1 (cat. no. sc-56030; 1:200) and FANCD2 (cat. no. sc-20022; 1:150) (both Santa Cruz Biotechnology, Inc., Dallas, TX, USA).

Techniques: Staining, Negative Control, Positive Control, Expressing

Expression of BRCA1 and FANCD2, and clinical characteristics of patients with BC.

Journal: Oncology Letters

Article Title: Expression and prognostic significance of Fanconi anemia group D2 protein and breast cancer type 1 susceptibility protein in familial and sporadic breast cancer

doi: 10.3892/ol.2019.10046

Figure Lengend Snippet: Expression of BRCA1 and FANCD2, and clinical characteristics of patients with BC.

Techniques: Expressing

Comparisons of (A) BRCA1 and (B) FANCD2 expression levels between breast cancer tissues and non-cancerous adjacent tissues. The red bar represents the tumor tissues and the gray bar indicates the non-cancerous adjacent tissues. These figures were derived from the Gene Expression Profiling Interactive Analysis dataset. *P<0.05. BRCA1, breast cancer type 1 susceptibility protein; FANCD2 Fanconi anemia group D2 protein.

Journal: Oncology Letters

Article Title: Expression and prognostic significance of Fanconi anemia group D2 protein and breast cancer type 1 susceptibility protein in familial and sporadic breast cancer

doi: 10.3892/ol.2019.10046

Figure Lengend Snippet: Comparisons of (A) BRCA1 and (B) FANCD2 expression levels between breast cancer tissues and non-cancerous adjacent tissues. The red bar represents the tumor tissues and the gray bar indicates the non-cancerous adjacent tissues. These figures were derived from the Gene Expression Profiling Interactive Analysis dataset. *P<0.05. BRCA1, breast cancer type 1 susceptibility protein; FANCD2 Fanconi anemia group D2 protein.

Techniques: Expressing, Derivative Assay, Gene Expression

Expression of BRCA1 and FANCD2, and clinical characteristics of patients with breast cancer obtained from The Cancer Genome Atlas dataset.

Journal: Oncology Letters

Article Title: Expression and prognostic significance of Fanconi anemia group D2 protein and breast cancer type 1 susceptibility protein in familial and sporadic breast cancer

doi: 10.3892/ol.2019.10046

Figure Lengend Snippet: Expression of BRCA1 and FANCD2, and clinical characteristics of patients with breast cancer obtained from The Cancer Genome Atlas dataset.

Techniques: Expressing

DFS of patients with breast cancer based on BRCA1 and FANCD2 expression. DFS of patients with FBC grouped by positive or negative expression of (A) BRCA1 and (B) FANCD2. DFS of patients with SBC were divided by positive or negative expression of (C) BRCA1 and (D) FANCD2. Probabilities of DFS were estimated using the Kaplan-Meier method and compared using the log-rank statistic. BRCA1, breast cancer type 1 susceptibility protein; FANCD2, Fanconi anemia group D2 protein; Cum, cumulative; DFS, disease-free survival; FBC, familial breast cancer; SBC, sporadic breast cancer.

Journal: Oncology Letters

Article Title: Expression and prognostic significance of Fanconi anemia group D2 protein and breast cancer type 1 susceptibility protein in familial and sporadic breast cancer

doi: 10.3892/ol.2019.10046

Figure Lengend Snippet: DFS of patients with breast cancer based on BRCA1 and FANCD2 expression. DFS of patients with FBC grouped by positive or negative expression of (A) BRCA1 and (B) FANCD2. DFS of patients with SBC were divided by positive or negative expression of (C) BRCA1 and (D) FANCD2. Probabilities of DFS were estimated using the Kaplan-Meier method and compared using the log-rank statistic. BRCA1, breast cancer type 1 susceptibility protein; FANCD2, Fanconi anemia group D2 protein; Cum, cumulative; DFS, disease-free survival; FBC, familial breast cancer; SBC, sporadic breast cancer.

Techniques: Expressing

Univariable and multivariable analyses of disease-free survival in the two groups of patients with breast cancer.

Journal: Oncology Letters

Article Title: Expression and prognostic significance of Fanconi anemia group D2 protein and breast cancer type 1 susceptibility protein in familial and sporadic breast cancer

doi: 10.3892/ol.2019.10046

Figure Lengend Snippet: Univariable and multivariable analyses of disease-free survival in the two groups of patients with breast cancer.

Techniques:

Western blot analysis of FANCD2 in patients with SBC. FANCD2 is represented by two adjacent bands. The upper stripe, L, is ubiquitinated FANCD2, and the lower stripe, S, is unubiquitinated FANCD2. Western blotting from the other 50 patients are shown in . BRCA1, breast cancer type 1 susceptibility protein; FANCD2, Fanconi anemia group D2 protein.

Journal: Oncology Letters

Article Title: Expression and prognostic significance of Fanconi anemia group D2 protein and breast cancer type 1 susceptibility protein in familial and sporadic breast cancer

doi: 10.3892/ol.2019.10046

Figure Lengend Snippet: Western blot analysis of FANCD2 in patients with SBC. FANCD2 is represented by two adjacent bands. The upper stripe, L, is ubiquitinated FANCD2, and the lower stripe, S, is unubiquitinated FANCD2. Western blotting from the other 50 patients are shown in . BRCA1, breast cancer type 1 susceptibility protein; FANCD2, Fanconi anemia group D2 protein.

Techniques: Western Blot

Journal: Nature Communications

Article Title: BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

doi: 10.1038/ncomms13398

Figure Lengend Snippet: ( a ) Viability curves for GBM01, GBM02 and GBM03 cells transduced with shCTRL virus or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4) (7 days). ( b ) Quantification of apoptotic cells (% of Annexin V-positive) for GBM01, GBM02 and GBM03 cells transduced with shCTRL virus or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( c ) Immunoblot analysis of BRCA1, caspase 3 and cleaved caspase-3 in GBM01 and GBM02 cells transduced with shCTRL virus or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). Tubulin was used as a loading control. ( d ) FACS analysis of cell cycle profile and the proliferative index (% of Edu-positive cells) in GBM01 cells transduced with shCTRL virus or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( e ) FACS analysis of cell cycle profile and the mitotic index (% of H3 Ser10 -positive cells) in DMSO or nocodazole treated GBM01 cells transduced with shCTRL virus or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( f ) Kaplan-Meier survival curve for NMRI nude mice intracranially injected with GBM01 or GBM03 cells transduced with shCTRL virus or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4 or shBRCA1-5). Statistical significance was calculated by one-way ANOVA, Tukey’s multiple comparisons test ( in vitro study) and Log-rank/Mantel-Cox test ( in vivo study). All data are shown as means±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Article Snippet: The sections were then incubated for 1 h with mouse monoclonal primary antibody against BRCA1 (1:200, IHC-00278, Bethyl Laboratories, Montgomery, TX), RRM2 (1:500, Abcam, ab57653) or Ki67 (DAKO) and followed with Dako EnVision+ Dual Link System-HRP secondary antibody (DAKO, Glostrup, Denmark) incubation for 1 h at room temperature.

Techniques: Transduction, Virus, Western Blot, Control, Injection, In Vitro, In Vivo

( a ) Microscopy analysis and quantification of pRPA mean signal intensity (in S phase) in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( b ) Microscopy analysis and quantification of Rad51 mean signal intensity (S phase) in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( c ) Microscopy analysis and quantification of 53BP1 foci count (G1 phase) in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( d ) Immunoblot analysis of DDR activation in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). * Chk1Ser317; # Chk1Ser345. ( e ) FACS quantification of double-positive p-RPA/γH2AX GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( f ) FACS quantification of double-positive PCNA/γH2AX GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( g ) Microscopy analysis and quantification of γH2AXfoci count in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( h ) Comet assay and tail moment quantification of DSBs in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test in a – c , e – h and all data are shown as means ±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Journal: Nature Communications

Article Title: BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

doi: 10.1038/ncomms13398

Figure Lengend Snippet: ( a ) Microscopy analysis and quantification of pRPA mean signal intensity (in S phase) in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( b ) Microscopy analysis and quantification of Rad51 mean signal intensity (S phase) in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( c ) Microscopy analysis and quantification of 53BP1 foci count (G1 phase) in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( d ) Immunoblot analysis of DDR activation in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). * Chk1Ser317; # Chk1Ser345. ( e ) FACS quantification of double-positive p-RPA/γH2AX GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( f ) FACS quantification of double-positive PCNA/γH2AX GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( g ) Microscopy analysis and quantification of γH2AXfoci count in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( h ) Comet assay and tail moment quantification of DSBs in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test in a – c , e – h and all data are shown as means ±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Techniques: Microscopy, Transduction, Western Blot, Activation Assay, Single Cell Gel Electrophoresis

( a ) DNA fibre assay measuring the replication fork progression speed in GBM cells (GBM01 and GBM02) transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). See also Table 1. ( b ) Replication fork recovery assay showing the quantification of CldU tract length in GBM01 cells transduced with shCTRL or 2 non-overlapping BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4) and treated or not with 2 mM HU (4 h) prior CldU labelling. See also Table 2; . ( c ) Immunoblot analysis of RRM2 protein levels in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( d , e ) RT-qPCR analysis of BRCA1 and RRM2 mRNA levels in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( f ) FACS analysis of RRM2 protein level changes throughout cell cycle in GBM cells (GBM01) transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( g ) Partial sequence of the human RRM2 promoter (GenBank accession number AY032750) , which was used to design Chip primers: P1 primer forward (F)/reverse (R) and P2 primer forward (F)/reverse (R). Positions are numbered from the downstream transcription initiation site (+1). Putative binding sites for transcription factors are color-coded and identified above the sequence. ( h ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in GBM01-03 cells using primer set P1 and P2. ( i ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in NHA-DRB and BJ cells using primer set P1 and P2. ( j ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in PC3, HELA, OVCAR and Cal51 cells using primer set P1 and P2. Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test in d – f , h – j or Student’s t test ( a , b ) and all data are shown as means±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Journal: Nature Communications

Article Title: BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

doi: 10.1038/ncomms13398

Figure Lengend Snippet: ( a ) DNA fibre assay measuring the replication fork progression speed in GBM cells (GBM01 and GBM02) transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). See also Table 1. ( b ) Replication fork recovery assay showing the quantification of CldU tract length in GBM01 cells transduced with shCTRL or 2 non-overlapping BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4) and treated or not with 2 mM HU (4 h) prior CldU labelling. See also Table 2; . ( c ) Immunoblot analysis of RRM2 protein levels in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( d , e ) RT-qPCR analysis of BRCA1 and RRM2 mRNA levels in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( f ) FACS analysis of RRM2 protein level changes throughout cell cycle in GBM cells (GBM01) transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( g ) Partial sequence of the human RRM2 promoter (GenBank accession number AY032750) , which was used to design Chip primers: P1 primer forward (F)/reverse (R) and P2 primer forward (F)/reverse (R). Positions are numbered from the downstream transcription initiation site (+1). Putative binding sites for transcription factors are color-coded and identified above the sequence. ( h ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in GBM01-03 cells using primer set P1 and P2. ( i ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in NHA-DRB and BJ cells using primer set P1 and P2. ( j ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in PC3, HELA, OVCAR and Cal51 cells using primer set P1 and P2. Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test in d – f , h – j or Student’s t test ( a , b ) and all data are shown as means±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Techniques: Transduction, Western Blot, Quantitative RT-PCR, Sequencing, Binding Assay, Immunoprecipitation

( a ) Luciferase assay of transcriptional activation of the RRM2 promoter in GBM01 transduced with shCTRL or shBRCA1-2/shBRCA1-4. ( b ) Luciferase assay of transcriptional activation of the RRM2 promoter in GBM01 after siRNA-mediated knockdown of Sp1; AP-1 and E2F1 in comparison to BRCA1. ( c ) Luciferase assay of transcriptional activation of the RRM2 promoter in GBM01 after siRNA-mediated knockdown of BRCA1 and E2F1 alone or on combination. ( d ) Chip immunoprecipitation of E2F1 binding RRM2 promoter in GBM01 cells using primer set P1 and P2. ( e ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in GBM01 cells transfected with siCTRL and siE2F1 using primer set P1 and P2. ( f ) DNA fibre assay measuring the replication fork progression speed in GBM cells lacking BRCA1 (shBRCA1-2 and shBRCA1-4) or not (shCTRL) transfected with either control vector (pcDNA) or vector expressing RRM2 (pcDNA-RRM2). See also Table 3. ( g ) Cell viability of GBM cells lacking BRCA1 (shBRCA1-2 and shBRCA1-4) or not (shCTRL) transfected with either control vector (pcDNA) or vector expressing RRM2 (pcDNA-RRM2). ( h ) Immunoblot analysis of BRCA1, p-RPA, RPA and RRM2 in GBM cells lacking BRCA1 (shBRCA1-2 and shBRCA1-4) or not (shCTRL) transfected with either control vector (pcDNA) or vector expressing RRM2 (pcDNA-RRM2). ( i ) Viability-based assessment of EC 50 triapine concentrations in GBM01, GBM02 and GBM03 cells. ( j ) DNA fibre assay measuring the replication fork progression speed in GBM cells treated with DMSO or EC 50 triapine. See also Table 4. Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test in a – d , f , h or Student’s t test ( e , i ) and all data are shown as means ±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Journal: Nature Communications

Article Title: BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

doi: 10.1038/ncomms13398

Figure Lengend Snippet: ( a ) Luciferase assay of transcriptional activation of the RRM2 promoter in GBM01 transduced with shCTRL or shBRCA1-2/shBRCA1-4. ( b ) Luciferase assay of transcriptional activation of the RRM2 promoter in GBM01 after siRNA-mediated knockdown of Sp1; AP-1 and E2F1 in comparison to BRCA1. ( c ) Luciferase assay of transcriptional activation of the RRM2 promoter in GBM01 after siRNA-mediated knockdown of BRCA1 and E2F1 alone or on combination. ( d ) Chip immunoprecipitation of E2F1 binding RRM2 promoter in GBM01 cells using primer set P1 and P2. ( e ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in GBM01 cells transfected with siCTRL and siE2F1 using primer set P1 and P2. ( f ) DNA fibre assay measuring the replication fork progression speed in GBM cells lacking BRCA1 (shBRCA1-2 and shBRCA1-4) or not (shCTRL) transfected with either control vector (pcDNA) or vector expressing RRM2 (pcDNA-RRM2). See also Table 3. ( g ) Cell viability of GBM cells lacking BRCA1 (shBRCA1-2 and shBRCA1-4) or not (shCTRL) transfected with either control vector (pcDNA) or vector expressing RRM2 (pcDNA-RRM2). ( h ) Immunoblot analysis of BRCA1, p-RPA, RPA and RRM2 in GBM cells lacking BRCA1 (shBRCA1-2 and shBRCA1-4) or not (shCTRL) transfected with either control vector (pcDNA) or vector expressing RRM2 (pcDNA-RRM2). ( i ) Viability-based assessment of EC 50 triapine concentrations in GBM01, GBM02 and GBM03 cells. ( j ) DNA fibre assay measuring the replication fork progression speed in GBM cells treated with DMSO or EC 50 triapine. See also Table 4. Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test in a – d , f , h or Student’s t test ( e , i ) and all data are shown as means ±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Techniques: Luciferase, Activation Assay, Transduction, Knockdown, Comparison, Immunoprecipitation, Binding Assay, Transfection, Control, Plasmid Preparation, Expressing, Western Blot

( a ) IHC staining of BRCA1 in normal brain (NB), WHO gr. II, III, IV glioma. Shown are representative sections. Scale bar 50 μm. ( b ) Quantification of ( a ) BRCA1 staining. Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test. ( c ) A survival curve for BRCA1 negative ( n =32); BRCA1 low (< 14.5% of BRCA1 + cells, n =35) or BRCA1 high (>14.5% of BRCA1 + cells, n =78; median survival of 230 days) glioma patients; Log-rank P value=0.00. Median survival for BRCA1 negative and low patient is not available as >50% of patients were alive at the end of study. ( d ) A survival curve for BRCA1 high (>14.5% of BRCA1 + cells, n =60, median survival of 159 days) and BRCA1 low (<14.5% of BRCA1 + cells, n =15; median survival of 251 days) GBM patients. Log-rank P -value=0.293. ( e ) Quantification of RRM2 staining (% of positive cells). Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test. ( f ) A survival curve for RRM2 negative ( n =64) and RRM2 positive ( n =81; median survival of 222 days) glioma patients, where the median RRM2-positivity is 1% and Log-rank P value=0.00. Median survival for RRM2 negative patients is not available as more than 50% of patients were alive at the end of study. ( g ) A survival curve for RRM2 positive ( n =56, median survival of 148 days) and RRM2 negative ( n =19; median survival of 320 days) GBM patients. Log-rank P value=0.23. ( h ) Spearman correlation test confirmed a positive correlation between the percentage of BRCA1 and RRM2-positive cells in human gliomas (our study dataset). ( i ) Spearman correlation test confirmed a positive correlation between BRCA1 and RRM2 mRNA expression in human gliomas (REMBRANDT dataset). (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Journal: Nature Communications

Article Title: BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

doi: 10.1038/ncomms13398

Figure Lengend Snippet: ( a ) IHC staining of BRCA1 in normal brain (NB), WHO gr. II, III, IV glioma. Shown are representative sections. Scale bar 50 μm. ( b ) Quantification of ( a ) BRCA1 staining. Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test. ( c ) A survival curve for BRCA1 negative ( n =32); BRCA1 low (< 14.5% of BRCA1 + cells, n =35) or BRCA1 high (>14.5% of BRCA1 + cells, n =78; median survival of 230 days) glioma patients; Log-rank P value=0.00. Median survival for BRCA1 negative and low patient is not available as >50% of patients were alive at the end of study. ( d ) A survival curve for BRCA1 high (>14.5% of BRCA1 + cells, n =60, median survival of 159 days) and BRCA1 low (<14.5% of BRCA1 + cells, n =15; median survival of 251 days) GBM patients. Log-rank P -value=0.293. ( e ) Quantification of RRM2 staining (% of positive cells). Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test. ( f ) A survival curve for RRM2 negative ( n =64) and RRM2 positive ( n =81; median survival of 222 days) glioma patients, where the median RRM2-positivity is 1% and Log-rank P value=0.00. Median survival for RRM2 negative patients is not available as more than 50% of patients were alive at the end of study. ( g ) A survival curve for RRM2 positive ( n =56, median survival of 148 days) and RRM2 negative ( n =19; median survival of 320 days) GBM patients. Log-rank P value=0.23. ( h ) Spearman correlation test confirmed a positive correlation between the percentage of BRCA1 and RRM2-positive cells in human gliomas (our study dataset). ( i ) Spearman correlation test confirmed a positive correlation between BRCA1 and RRM2 mRNA expression in human gliomas (REMBRANDT dataset). (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Techniques: Immunohistochemistry, Staining, Expressing

Putative miR-15/107 targets within the BRCA1 CDS. (A) Schematic representation of protein-coding BRCA1 transcript. (B) Density function and cumulative distribution of CDS length across all human coding mRNAs. (C) The rna22-predicted target site for the miR-15/107 group together with the corresponding miRNA:mRNA heteroduplexes.

Journal: Frontiers in Genetics

Article Title: Post-transcriptional regulation of BRCA1 through its coding sequence by the miR-15/107 group of miRNAs

doi: 10.3389/fgene.2015.00242

Figure Lengend Snippet: Putative miR-15/107 targets within the BRCA1 CDS. (A) Schematic representation of protein-coding BRCA1 transcript. (B) Density function and cumulative distribution of CDS length across all human coding mRNAs. (C) The rna22-predicted target site for the miR-15/107 group together with the corresponding miRNA:mRNA heteroduplexes.

Article Snippet: Primary antibodies include anti-BRCA1 (D54A8, Cell Signaling, Danvers, MA, USA) and anti-β-actin (8H10D10, Cell Signaling).

Techniques:

Suppression of BRCA1 mRNA by miR-15/107 miRNAs. Cell lines transfected with miR-15/107 miRNA precursors show a significant decrease in the amount of available BRCA1 transcript 48 h post-transfection as detected by qRT-PCR. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 compared to control scramble miR by Student’s t -test, n = 3 in each group.

Journal: Frontiers in Genetics

Article Title: Post-transcriptional regulation of BRCA1 through its coding sequence by the miR-15/107 group of miRNAs

doi: 10.3389/fgene.2015.00242

Figure Lengend Snippet: Suppression of BRCA1 mRNA by miR-15/107 miRNAs. Cell lines transfected with miR-15/107 miRNA precursors show a significant decrease in the amount of available BRCA1 transcript 48 h post-transfection as detected by qRT-PCR. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 compared to control scramble miR by Student’s t -test, n = 3 in each group.

Article Snippet: Primary antibodies include anti-BRCA1 (D54A8, Cell Signaling, Danvers, MA, USA) and anti-β-actin (8H10D10, Cell Signaling).

Techniques: Transfection, Quantitative RT-PCR, Control

Characterization of a novel miR-15/107 target site within the BRCA1 CDS. The putative binding site for the miR-15/107 group in BRCA1’s CDS was cloned into a luciferase reporter vector along with a corresponding construct containing mutations within the putative miRNA ‘seed’ recognition sites to confirm specificity. ∗ P < 0.05, ∗∗ P < 0.01 compared to control scramble target sequence by Student’s t -test, n = 3 in each group.

Journal: Frontiers in Genetics

Article Title: Post-transcriptional regulation of BRCA1 through its coding sequence by the miR-15/107 group of miRNAs

doi: 10.3389/fgene.2015.00242

Figure Lengend Snippet: Characterization of a novel miR-15/107 target site within the BRCA1 CDS. The putative binding site for the miR-15/107 group in BRCA1’s CDS was cloned into a luciferase reporter vector along with a corresponding construct containing mutations within the putative miRNA ‘seed’ recognition sites to confirm specificity. ∗ P < 0.05, ∗∗ P < 0.01 compared to control scramble target sequence by Student’s t -test, n = 3 in each group.

Article Snippet: Primary antibodies include anti-BRCA1 (D54A8, Cell Signaling, Danvers, MA, USA) and anti-β-actin (8H10D10, Cell Signaling).

Techniques: Binding Assay, Clone Assay, Luciferase, Plasmid Preparation, Construct, Control, Sequencing

Sequestration of miR-15/107 miRNAs impacts BRCA1 mRNA. Cells transfected with luciferase reporter plasmids containing antisense (as) miRNA sequences or predicted wild type (WT) BRCA1 miR-15/107 MRE demonstrate varying levels of BRCA1 expression rescue. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 compared to control by Student’s t -test, n = 3 in each group.

Journal: Frontiers in Genetics

Article Title: Post-transcriptional regulation of BRCA1 through its coding sequence by the miR-15/107 group of miRNAs

doi: 10.3389/fgene.2015.00242

Figure Lengend Snippet: Sequestration of miR-15/107 miRNAs impacts BRCA1 mRNA. Cells transfected with luciferase reporter plasmids containing antisense (as) miRNA sequences or predicted wild type (WT) BRCA1 miR-15/107 MRE demonstrate varying levels of BRCA1 expression rescue. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 compared to control by Student’s t -test, n = 3 in each group.

Article Snippet: Primary antibodies include anti-BRCA1 (D54A8, Cell Signaling, Danvers, MA, USA) and anti-β-actin (8H10D10, Cell Signaling).

Techniques: Transfection, Luciferase, Expressing, Control

Translational suppression of BRCA1 by miR-15/107 miRNAs. Western immunoblots from hTERT-HPNE, HCT-116, and MIA PaCa-2 cells demonstrate relative levels of BRCA1 protein expression at 72 h post-transfection with control scramble miRNA and anti-miR precursors, miRNA and anti-miR precursors, or siBRCA1 control.

Journal: Frontiers in Genetics

Article Title: Post-transcriptional regulation of BRCA1 through its coding sequence by the miR-15/107 group of miRNAs

doi: 10.3389/fgene.2015.00242

Figure Lengend Snippet: Translational suppression of BRCA1 by miR-15/107 miRNAs. Western immunoblots from hTERT-HPNE, HCT-116, and MIA PaCa-2 cells demonstrate relative levels of BRCA1 protein expression at 72 h post-transfection with control scramble miRNA and anti-miR precursors, miRNA and anti-miR precursors, or siBRCA1 control.

Article Snippet: Primary antibodies include anti-BRCA1 (D54A8, Cell Signaling, Danvers, MA, USA) and anti-β-actin (8H10D10, Cell Signaling).

Techniques: Western Blot, Expressing, Transfection, Control

A. Expression of BRCA1 was analysed by Western blotting using anti-BRCA1 antibody. Mouse anti-BRCA1 primary antibody was purchased from Oncogene Research (San Diego, CA). Actin was used as a loading control. B. Proliferation experiments were performed using the Sulforhodamine B technique. Data are means of three independent experiments + SEM. C. Cycle distribution was determined using flow cytometry. Data are means of three independent experiments + SEM. D. Percentage of apoptotic cells was determined at 48 h using the Annexin V test. Data are presented as means of 3 independent replicates + SEM. *: p<0.05.

Journal: PLoS ONE

Article Title: BRCA1 Induces Major Energetic Metabolism Reprogramming in Breast Cancer Cells

doi: 10.1371/journal.pone.0102438

Figure Lengend Snippet: A. Expression of BRCA1 was analysed by Western blotting using anti-BRCA1 antibody. Mouse anti-BRCA1 primary antibody was purchased from Oncogene Research (San Diego, CA). Actin was used as a loading control. B. Proliferation experiments were performed using the Sulforhodamine B technique. Data are means of three independent experiments + SEM. C. Cycle distribution was determined using flow cytometry. Data are means of three independent experiments + SEM. D. Percentage of apoptotic cells was determined at 48 h using the Annexin V test. Data are presented as means of 3 independent replicates + SEM. *: p<0.05.

Article Snippet: Mouse OP92 (Ab-1) anti-BRCA1 primary antibody was purchased from Oncogene Research (San Diego, CA).

Techniques: Expressing, Western Blot, Control, Flow Cytometry

A. Gene expression study: mRNA of SUM1315-LXSN and SUM1315-BRCA1 cells were extracted and analyzed on TaqMan Low Density Arrays as described in materials and methods. The replicates represent independent culture experiments. Low levels of expression are represented in blue and high levels of expression in yellow. B. The major metabolites observed by 1 H-NMR and by LC-MS were analyzed by hierarchical clustering . The replicates represent independent culture experiments. Small quantities of metabolites are represented in blue and high quantities in yellow.

Journal: PLoS ONE

Article Title: BRCA1 Induces Major Energetic Metabolism Reprogramming in Breast Cancer Cells

doi: 10.1371/journal.pone.0102438

Figure Lengend Snippet: A. Gene expression study: mRNA of SUM1315-LXSN and SUM1315-BRCA1 cells were extracted and analyzed on TaqMan Low Density Arrays as described in materials and methods. The replicates represent independent culture experiments. Low levels of expression are represented in blue and high levels of expression in yellow. B. The major metabolites observed by 1 H-NMR and by LC-MS were analyzed by hierarchical clustering . The replicates represent independent culture experiments. Small quantities of metabolites are represented in blue and high quantities in yellow.

Article Snippet: Mouse OP92 (Ab-1) anti-BRCA1 primary antibody was purchased from Oncogene Research (San Diego, CA).

Techniques: Gene Expression, Expressing, Liquid Chromatography with Mass Spectroscopy

A. The major enzymes and metabolites involved in energy metabolism were quantified by q-RT-PCR, 1 H-NMR and by LC-MS. Data are presented as means of at least 3 independent replicates + SEM. *: p<0.05; **: p<0.01, +: p = 0.06 for lactate, SUM1315-BRCA1 vs SUM1315-LXSN cell lines. B. Analyses of HK2 and IDH1 enzymes was performed by Western Blot and quantified by ImageJ software. Data are presented as means of 3 independent replicates + SEM. *: p<0.05; ***: p<0.001, SUM1315-BRCA1 vs SUM1315-LXSN cell lines. C. The oxygen partial pressure was measured in the culture medium of SUM1315-LXSN and SUM1315-BRCA1 cell lines subjected to hypoxic atmosphere for the indicated time. *: p<0.05, SUM1315-BRCA1 vs SUM1315-LXSN cell lines. D. Production of lactate and consumption of glucose were measured in cell culture media by enzymatic colorimetric assays. Data are presented as means of 3 independent replicates + SEM.

Journal: PLoS ONE

Article Title: BRCA1 Induces Major Energetic Metabolism Reprogramming in Breast Cancer Cells

doi: 10.1371/journal.pone.0102438

Figure Lengend Snippet: A. The major enzymes and metabolites involved in energy metabolism were quantified by q-RT-PCR, 1 H-NMR and by LC-MS. Data are presented as means of at least 3 independent replicates + SEM. *: p<0.05; **: p<0.01, +: p = 0.06 for lactate, SUM1315-BRCA1 vs SUM1315-LXSN cell lines. B. Analyses of HK2 and IDH1 enzymes was performed by Western Blot and quantified by ImageJ software. Data are presented as means of 3 independent replicates + SEM. *: p<0.05; ***: p<0.001, SUM1315-BRCA1 vs SUM1315-LXSN cell lines. C. The oxygen partial pressure was measured in the culture medium of SUM1315-LXSN and SUM1315-BRCA1 cell lines subjected to hypoxic atmosphere for the indicated time. *: p<0.05, SUM1315-BRCA1 vs SUM1315-LXSN cell lines. D. Production of lactate and consumption of glucose were measured in cell culture media by enzymatic colorimetric assays. Data are presented as means of 3 independent replicates + SEM.

Article Snippet: Mouse OP92 (Ab-1) anti-BRCA1 primary antibody was purchased from Oncogene Research (San Diego, CA).

Techniques: Reverse Transcription Polymerase Chain Reaction, Liquid Chromatography with Mass Spectroscopy, Western Blot, Software, Cell Culture

A. The major enzymes and metabolites involved in antioxidation metabolism were quantified by q-RT-PCR, 1 H-NMR and by LC-MS. Data are presented as means of at least 3 independent replicates + SEM. *: p<0.05; **: p<0.01, SUM1315-BRCA1 vs SUM1315-LXSN cell lines. B. Schematic representation of glutathione metabolism and its regulation by BRCA1. Genes ( italicized ) in red: overexpression. Metabolites: grey, not detected; red, increased.

Journal: PLoS ONE

Article Title: BRCA1 Induces Major Energetic Metabolism Reprogramming in Breast Cancer Cells

doi: 10.1371/journal.pone.0102438

Figure Lengend Snippet: A. The major enzymes and metabolites involved in antioxidation metabolism were quantified by q-RT-PCR, 1 H-NMR and by LC-MS. Data are presented as means of at least 3 independent replicates + SEM. *: p<0.05; **: p<0.01, SUM1315-BRCA1 vs SUM1315-LXSN cell lines. B. Schematic representation of glutathione metabolism and its regulation by BRCA1. Genes ( italicized ) in red: overexpression. Metabolites: grey, not detected; red, increased.

Article Snippet: Mouse OP92 (Ab-1) anti-BRCA1 primary antibody was purchased from Oncogene Research (San Diego, CA).

Techniques: Reverse Transcription Polymerase Chain Reaction, Liquid Chromatography with Mass Spectroscopy, Over Expression

A. The major enzymes and metabolites involved in lipid metabolism were quantified by 1 H-NMR, quantitative RT-PCR and HPTLC. Data are presented as means of at least 3 independent replicates + SEM. *: p<0.05; **: p<0.01, SUM1315-BRCA1 vs SUM1315-LXSN cell lines. BOHButyrate: β-hydroxybutyrate. B. Intact whole cell pellets were analyzed by 1 H-NMR spectroscopy in order to reveal differential metabolites the most concentrated in breast tumor cells. Spectra were normalized according to a published procedure . Representative spectra of intact SUM1315-LXSN (blue) and SUM1315-BRCA1 (red) cells are shown. Arrows: most concentrated differential signals. C. Fatty acid composition was analyzed by GCFS. Results of major groups are given as percentage of total lipids. Data are presented as means of at least 3 independent replicates + SEM. *: p<0.05; **: p<0.02, SUM1315-BRCA1 vs SUM1315-LXSN cell lines.

Journal: PLoS ONE

Article Title: BRCA1 Induces Major Energetic Metabolism Reprogramming in Breast Cancer Cells

doi: 10.1371/journal.pone.0102438

Figure Lengend Snippet: A. The major enzymes and metabolites involved in lipid metabolism were quantified by 1 H-NMR, quantitative RT-PCR and HPTLC. Data are presented as means of at least 3 independent replicates + SEM. *: p<0.05; **: p<0.01, SUM1315-BRCA1 vs SUM1315-LXSN cell lines. BOHButyrate: β-hydroxybutyrate. B. Intact whole cell pellets were analyzed by 1 H-NMR spectroscopy in order to reveal differential metabolites the most concentrated in breast tumor cells. Spectra were normalized according to a published procedure . Representative spectra of intact SUM1315-LXSN (blue) and SUM1315-BRCA1 (red) cells are shown. Arrows: most concentrated differential signals. C. Fatty acid composition was analyzed by GCFS. Results of major groups are given as percentage of total lipids. Data are presented as means of at least 3 independent replicates + SEM. *: p<0.05; **: p<0.02, SUM1315-BRCA1 vs SUM1315-LXSN cell lines.

Article Snippet: Mouse OP92 (Ab-1) anti-BRCA1 primary antibody was purchased from Oncogene Research (San Diego, CA).

Techniques: Quantitative RT-PCR, High Performance Thin Layer Chromatography, Structural Proteomics

Enzymes or metabolites up-regulated in SUM1315-BRCA1 cells compared to SUM1315-LXSN cells are represented in red whereas down-regulated ones are presented in green.

Journal: PLoS ONE

Article Title: BRCA1 Induces Major Energetic Metabolism Reprogramming in Breast Cancer Cells

doi: 10.1371/journal.pone.0102438

Figure Lengend Snippet: Enzymes or metabolites up-regulated in SUM1315-BRCA1 cells compared to SUM1315-LXSN cells are represented in red whereas down-regulated ones are presented in green.

Article Snippet: Mouse OP92 (Ab-1) anti-BRCA1 primary antibody was purchased from Oncogene Research (San Diego, CA).

Techniques:

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