PDF DatasheetHuman Anti-BRCA1 Antibody Product Attributes
BRCA1 Previously Observed Antibody Staining Patterns
Observed Antibody Staining Data By Tissue Type:
Variations in BRCA1 antibody staining intensity in immunohistochemistry on tissue sections are present across different anatomical locations. An intense signal was observed in epidermal cells in the skin and germinal center cells in the lymph node. More moderate antibody staining intensity was present in epidermal cells in the skin and germinal center cells in the lymph node. Low, but measureable presence of BRCA1 could be seen inadipocytes in breast and mesenchymal tissue, bile duct cells in the liver, cells in the endometrial stroma in endometrium, cells in the granular layer in cerebellum, cells in the molecular layer in cerebellum, cells in the red pulp in spleen, chondrocytes in mesenchymal tissue, endothelial cells in the colon, fibroblasts in mesenchymal tissue, glandular cells in the salivary gland, glial cells in the caudate nucleus, cerebral cortex and hippocampus, hepatocytes in liver, myocytes in heart muscle and skeletal muscle, neuronal cells in the hippocampus, neuropil in cerebral cortex, ovarian stroma cells in the ovary, peripheral nerve in mesenchymal tissue, peripheral nerve/ganglion in colon and smooth muscle cells in the smooth muscle. We were unable to detect BRCA1 in other tissues. Disease states, inflammation, and other physiological changes can have a substantial impact on antibody staining patterns. These measurements were all taken in tissues deemed normal or from patients without known disease.
Observed Antibody Staining Data By Tissue Disease Status:
Tissues from cancer patients, for instance, have their own distinct pattern of BRCA1 expression as measured by anti-BRCA1 antibody immunohistochemical staining. The average level of expression by tumor is summarized in the table below. The variability row represents patient to patient variability in IHC staining.
| Sample Type | breast cancer | carcinoid | cervical cancer | colorectal cancer | endometrial cancer | glioma | head and neck cancer | liver cancer | lung cancer | lymphoma | melanoma | ovarian cancer | pancreatic cancer | prostate cancer | renal cancer | skin cancer | stomach cancer | testicular cancer | thyroid cancer | urothelial cancer |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Signal Intensity | ++ | + | ++ | ++ | – | ++ | ++ | + | – | + | ++ | + | + | + | – | + | + | ++ | ++ | ++ |
| BRCA1 Variability | +++ | ++ | ++ | + | ++ | ++ | ++ | + | ++ | +++ | ++ | ++ | + | ++ | ++ | ++ | ++ | ++ | ++ | ++ |
| BRCA1 General Information | |
|---|---|
| Alternate Names | |
| BRCA1, breast cancer type 1 susceptibility protein, breast cancer 1 | |
| Molecular Weight | |
| 220kDa | |
| Chromosomal Location | |
| 17q21 | |
| Curated Database and Bioinformatic Data | |
| Gene Symbol | BRCA1 |
| Entrez Gene ID | 672 |
| Ensemble Gene ID | ENSG00000012048 |
| RefSeq Protein Accession(s) | NP_009225, NP_009230, NP_009228, NP_009231, NP_009229 |
| RefSeq mRNA Accession(s) | NM_007298, NM_007296 NM_007297, NM_007295, NM_007300, NM_007303, NM_007306, NM_007301, NM_007302, NM_007305, NM_007294, NM_007299, NR_027676 |
| RefSeq Genomic Accession(s) | NC_018928, NC_000017, NG_005905 |
| UniProt ID(s) | A0A024R1V0, P38398 |
| UniGene ID(s) | A0A024R1V0, P38398 |
| HGNC ID(s) | 1100 |
| Cosmic ID(s) | BRCA1 |
| KEGG Gene ID(s) | hsa:672 |
| PharmGKB ID(s) | PA25411 |
| General Description of BRCA1. | |
| This gene encodes a nuclear phosphoprotein that plays a role in maintaining genomic stability, and it also acts as a tumor suppressor. The encoded protein combines with other tumor suppressors, DNA damage sensors, and signal transducers to form a large multi-subunit protein complex known as the BRCA1-associated genome surveillance complex (BASC). This gene product associates with RNA polymerase II, and through the C-terminal domain, also interacts with histone deacetylase complexes. This protein thus plays a role in transcription, DNA repair of double-stranded breaks, and recombination. Mutations in this gene are responsible for approximately 40% of inherited breast cancers and more than 80% of inherited breast and ovarian cancers. Alternative splicing plays a role in modulating the subcellular localization and physiological function of this gene. | |
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