
抗人 CDK2AP1 抗体对
01AB03363
Cyclin dependent kinase 2 associated protein 1 (CDK2AP1), also known as DOC1, is a tumor suppressor protein that regulates the G1-to-S phase transition and DNA replication. It functions primarily by sequestering monomeric CDK2 and targeting it for proteolysis, while also interacting with DNA polymerase alpha/primase to modulate genomic stability. Structurally, the protein forms a homodimer featuring an intrinsically disordered N-terminal region and a C-terminal four-helix bundle. Beyond its role in cell cycle control, CDK2AP1 serves as a core component of the nucleosome remodeling and deacetylase (NuRD) complex, where it facilitates the epigenetic silencing of pluripotency genes and promotes cellular differentiation. Clinically, the downregulation of CDK2AP1 is frequently observed in oral, breast, and prostate cancers, as well as gliomas. Its loss is associated with increased cellular proliferation and invasion, highlighting its importance in maintaining normal growth constraints.
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技术参数
- 靶点基因名
- CDK2AP1
- 基因别名
- CDKAP1; DOC1
- 蛋白别名
- cyclin dependent kinase 2 associated protein 1; CDK2AP1
- UniProt
- O14519
- 物种
- Human
产品详情
- 靶点名称
- CDK2AP1
- 蛋白名称
- cyclin dependent kinase 2 associated protein 1
- 蛋白别名
- Cyclin-dependent kinase 2-associated protein 1; CDK2-associated protein 1; Deleted in oral cancer 1; DOC-1; Putative oral cancer suppressor
- 靶点基因名
- CDK2AP1
- 基因别名
- CDKAP1; DOC1
- UniProt
- O14519
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Cyclin dependent kinase 2 associated protein 1 (CDK2AP1), also known as DOC1, is a tumor suppressor protein that regulates the G1-to-S phase transition and DNA replication. It functions primarily by sequestering monomeric CDK2 and targeting it for proteolysis, while also interacting with DNA polymerase alpha/primase to modulate genomic stability. Structurally, the protein forms a homodimer featuring an intrinsically disordered N-terminal region and a C-terminal four-helix bundle. Beyond its role in cell cycle control, CDK2AP1 serves as a core component of the nucleosome remodeling and deacetylase (NuRD) complex, where it facilitates the epigenetic silencing of pluripotency genes and promotes cellular differentiation. Clinically, the downregulation of CDK2AP1 is frequently observed in oral, breast, and prostate cancers, as well as gliomas. Its loss is associated with increased cellular proliferation and invasion, highlighting its importance in maintaining normal growth constraints.