抗人 PBK/TOPK 抗体对
01AB02996
PDZ binding kinase (PBK), also known as T-LAK cell-originated protein kinase (TOPK), is a 322-amino acid serine/threonine kinase related to the MAPKK family, characterized by a C-terminal PDZ-binding motif and primarily active during mitosis. PBK is involved in cell cycle regulation, phosphorylating substrates such as p38 MAPK and histone H3, and is implicated in the activation of lymphoid cells and testicular function, including spermatogenesis. The protein is predominantly expressed in proliferative tissues and is upregulated in various cancers, including hematologic malignancies and solid tumors, where its overexpression correlates with advanced tumor stage, poor prognosis, and enhanced tumor cell proliferation, invasion, and immune escape. PBK promotes oncogenic processes by modulating signaling pathways such as p53, MAPK, and PI3K/AKT, and its inhibition suppresses tumor growth and metastasis, highlighting its potential as a therapeutic target in oncology.
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技术参数
- 靶点基因名
- PBK
- 基因别名
- TOPK
- 蛋白别名
- PDZ binding kinase; PBK/TOPK
- UniProt
- Q96KB5
- 物种
- Human
产品详情
- 靶点名称
- PBK/TOPK
- 蛋白名称
- PDZ binding kinase
- 蛋白别名
- Lymphokine-activated killer T-cell-originated protein kinase; Cancer/testis antigen 84; CT84; MAPKK-like protein kinase; Nori-3; PDZ-binding kinase; Spermatogenesis-related protein kinase; SPK; T-LAK cell-originated protein kinase
- 靶点基因名
- PBK
- 基因别名
- TOPK
- UniProt
- Q96KB5
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
PDZ binding kinase (PBK), also known as T-LAK cell-originated protein kinase (TOPK), is a 322-amino acid serine/threonine kinase related to the MAPKK family, characterized by a C-terminal PDZ-binding motif and primarily active during mitosis. PBK is involved in cell cycle regulation, phosphorylating substrates such as p38 MAPK and histone H3, and is implicated in the activation of lymphoid cells and testicular function, including spermatogenesis. The protein is predominantly expressed in proliferative tissues and is upregulated in various cancers, including hematologic malignancies and solid tumors, where its overexpression correlates with advanced tumor stage, poor prognosis, and enhanced tumor cell proliferation, invasion, and immune escape. PBK promotes oncogenic processes by modulating signaling pathways such as p53, MAPK, and PI3K/AKT, and its inhibition suppresses tumor growth and metastasis, highlighting its potential as a therapeutic target in oncology.