人 53BP1 抗体对
01AB00439
Tumor protein p53 binding protein 1 (TP53BP1) is a crucial protein involved in DNA double-strand break repair, particularly in promoting non-homologous end joining (NHEJ) pathways. It interacts with damaged chromatin, recognizing specific epigenetic markers, and plays a role in telomere dynamics and class-switch recombination during antibody genesis. TP53BP1 forms a complex with RIF1, inhibiting DNA end resection and competing with BRCA1-CtIP to determine the repair pathway choice. The protein contains multiple functional domains and exists in three cellular pools: cytoplasmic, nuclear, and DNA repair foci. TP53BP1 also binds to the p53 protein, regulating cell cycle progression and proliferation. In terms of disease relevance, TP53BP1 is underexpressed in most cases of triple-negative breast cancer. Additionally, as individuals age, the recruitment of 53BP1 to double-strand breaks during the G1 phase becomes deficient, potentially contributing to the aging process through error-prone repair mechanisms.
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技术参数
- 靶点基因名
- TP53BP1
- 蛋白别名
- tumor protein p53 binding protein 1; 53BP1
- UniProt
- Q12888
- 物种
- Human
产品详情
- 靶点名称
- 53BP1
- 蛋白名称
- tumor protein p53 binding protein 1
- 蛋白别名
- TP53-binding protein 1; 53BP1; p53-binding protein 1; p53BP1
- 靶点基因名
- TP53BP1
- UniProt
- Q12888
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Tumor protein p53 binding protein 1 (TP53BP1) is a crucial protein involved in DNA double-strand break repair, particularly in promoting non-homologous end joining (NHEJ) pathways. It interacts with damaged chromatin, recognizing specific epigenetic markers, and plays a role in telomere dynamics and class-switch recombination during antibody genesis. TP53BP1 forms a complex with RIF1, inhibiting DNA end resection and competing with BRCA1-CtIP to determine the repair pathway choice. The protein contains multiple functional domains and exists in three cellular pools: cytoplasmic, nuclear, and DNA repair foci. TP53BP1 also binds to the p53 protein, regulating cell cycle progression and proliferation. In terms of disease relevance, TP53BP1 is underexpressed in most cases of triple-negative breast cancer. Additionally, as individuals age, the recruitment of 53BP1 to double-strand breaks during the G1 phase becomes deficient, potentially contributing to the aging process through error-prone repair mechanisms.