
抗人 BRCA1 抗体对
01AB02385
BRCA1 DNA repair associated (BRCA1) is a nuclear tumor suppressor that functions as an E3 ubiquitin ligase in complex with BARD1. It plays a central role in maintaining genomic stability through DNA double-strand break repair via homologous recombination and genome surveillance. BRCA1 coordinates DNA damage sensing with repair and regulates S, G2/M, and G1/S cell-cycle checkpoints through interactions with proteins such as ATM, ATR, Chk1, and MDC1. Germline loss-of-function variants in BRCA1 are the primary cause of hereditary breast and ovarian cancer syndrome, significantly increasing the lifetime risk of breast, epithelial ovarian, fallopian tube, and peritoneal cancers. BRCA1-deficient cells exhibit chromosomal instability and hypersensitivity to DNA-damaging agents and PARP inhibitors, a vulnerability utilized in targeted oncological therapies.
| 规格 | 起售价 |
|---|---|
| 登录后可查看 | |
技术参数
- 靶点基因名
- BRCA1
- 基因别名
- RNF53
- 蛋白别名
- BRCA1 DNA repair associated; BRCA1
- UniProt
- P38398
- 物种
- Human
产品详情
- 靶点名称
- BRCA1
- 蛋白名称
- BRCA1 DNA repair associated
- 蛋白别名
- Breast cancer type 1 susceptibility protein; RING finger protein 53; RING-type E3 ubiquitin transferase BRCA1
- 靶点基因名
- BRCA1
- 基因别名
- RNF53
- UniProt
- P38398
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
BRCA1 DNA repair associated (BRCA1) is a nuclear tumor suppressor that functions as an E3 ubiquitin ligase in complex with BARD1. It plays a central role in maintaining genomic stability through DNA double-strand break repair via homologous recombination and genome surveillance. BRCA1 coordinates DNA damage sensing with repair and regulates S, G2/M, and G1/S cell-cycle checkpoints through interactions with proteins such as ATM, ATR, Chk1, and MDC1. Germline loss-of-function variants in BRCA1 are the primary cause of hereditary breast and ovarian cancer syndrome, significantly increasing the lifetime risk of breast, epithelial ovarian, fallopian tube, and peritoneal cancers. BRCA1-deficient cells exhibit chromosomal instability and hypersensitivity to DNA-damaging agents and PARP inhibitors, a vulnerability utilized in targeted oncological therapies.