人 PCLAF 抗体对
01AB02247
PCNA clamp associated factor (PCLAF), also known as KIAA0101 or PAF15, is a small, intrinsically disordered protein that binds to proliferating cell nuclear antigen (PCNA) via a conserved PIP box motif, playing a crucial role in DNA replication, repair, and cell cycle regulation. PCLAF acts as a molecular adaptor, facilitating the recruitment of DNA polymerases during replication and enabling translesion DNA synthesis to bypass DNA lesions, particularly after DNA damage disrupts its interaction with PCNA. It is primarily localized in the nucleus and centrosome, with expression tightly regulated during the cell cycle and rapidly degraded at mitotic exit. Overexpression of PCLAF is observed in numerous cancers, including gastrointestinal, liver, pancreatic, cervical, and anaplastic thyroid carcinomas, where it promotes tumorigenesis, cell proliferation, migration, invasion, and epithelial-mesenchymal transition, and is associated with poor prognosis. PCLAF is also implicated in tumor immune infiltration and is being explored as a potential molecular target for cancer therapeutics.
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技术参数
- 靶点基因名
- PCLAF
- 基因别名
- KIAA0101; NS5ATP9; PAF
- 蛋白别名
- PCNA clamp associated factor; PCLAF
- UniProt
- Q15004
- 物种
- Human
产品详情
- 靶点名称
- PCLAF
- 蛋白名称
- PCNA clamp associated factor
- 蛋白别名
- PCNA-associated factor; Hepatitis C virus NS5A-transactivated protein 9; HCV NS5A-transactivated protein 9; Overexpressed in anaplastic thyroid carcinoma 1; OEATC-1; PCNA-associated factor of 15 kDa; PAF15; p15PAF; PCNA-clamp-associated factor
- 靶点基因名
- PCLAF
- 基因别名
- KIAA0101; NS5ATP9; PAF
- UniProt
- Q15004
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
PCNA clamp associated factor (PCLAF), also known as KIAA0101 or PAF15, is a small, intrinsically disordered protein that binds to proliferating cell nuclear antigen (PCNA) via a conserved PIP box motif, playing a crucial role in DNA replication, repair, and cell cycle regulation. PCLAF acts as a molecular adaptor, facilitating the recruitment of DNA polymerases during replication and enabling translesion DNA synthesis to bypass DNA lesions, particularly after DNA damage disrupts its interaction with PCNA. It is primarily localized in the nucleus and centrosome, with expression tightly regulated during the cell cycle and rapidly degraded at mitotic exit. Overexpression of PCLAF is observed in numerous cancers, including gastrointestinal, liver, pancreatic, cervical, and anaplastic thyroid carcinomas, where it promotes tumorigenesis, cell proliferation, migration, invasion, and epithelial-mesenchymal transition, and is associated with poor prognosis. PCLAF is also implicated in tumor immune infiltration and is being explored as a potential molecular target for cancer therapeutics.