
人 PIP4K2A 抗体对
01AB01791
Phosphatidylinositol-5-phosphate 4-kinase type 2 alpha (PIP4K2A) is a lipid kinase that phosphorylates phosphatidylinositol-5-phosphate (PtdIns5P) to generate phosphatidylinositol-4,5-bisphosphate [PtdIns(4,5)P2]. By modulating these phosphoinositide pools, it regulates PI3K-AKT signaling, vesicle trafficking, and autophagy during nutrient stress. PIP4K2A also influences ciliogenesis by phosphorylating macrophage migration inhibitory factor (MIF). Clinically, PIP4K2A exhibits context-dependent roles in cancer; it acts as a tumor suppressor in PTEN-deficient glioblastoma by attenuating AKT signaling, whereas it is required for the maintenance of leukemia-initiating cells in acute myeloid leukemia. Its loss in leukemic contexts triggers cell-cycle arrest, highlighting its potential as a therapeutic target in specific hematological malignancies.
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技术参数
- 靶点基因名
- PIP4K2A
- 基因别名
- PI5P4KA; PIP5K2; PIP5K2A
- 蛋白别名
- phosphatidylinositol-5-phosphate 4-kinase type 2 alpha; PIP4K2A
- UniProt
- P48426
- 物种
- Human
产品详情
- 靶点名称
- PIP4K2A
- 蛋白名称
- phosphatidylinositol-5-phosphate 4-kinase type 2 alpha
- 蛋白别名
- Phosphatidylinositol 5-phosphate 4-kinase type-2 alpha; 1-phosphatidylinositol 5-phosphate 4-kinase 2-alpha; Diphosphoinositide kinase 2-alpha; PIP5KIII; Phosphatidylinositol 5-Phosphate 4-Kinase; PI5P4Kalpha; Phosphatidylinositol 5-phosphate 4-kinase type II alpha; PI(5)P 4-kinase type II alpha; PIP4KII-alpha; PtdIns(4)P-5-kinase B isoform; PtdIns(4)P-5-kinase C isoform; PtdIns(5)P-4-kinase isoform 2-alpha
- 靶点基因名
- PIP4K2A
- 基因别名
- PI5P4KA; PIP5K2; PIP5K2A
- UniProt
- P48426
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Phosphatidylinositol-5-phosphate 4-kinase type 2 alpha (PIP4K2A) is a lipid kinase that phosphorylates phosphatidylinositol-5-phosphate (PtdIns5P) to generate phosphatidylinositol-4,5-bisphosphate [PtdIns(4,5)P2]. By modulating these phosphoinositide pools, it regulates PI3K-AKT signaling, vesicle trafficking, and autophagy during nutrient stress. PIP4K2A also influences ciliogenesis by phosphorylating macrophage migration inhibitory factor (MIF). Clinically, PIP4K2A exhibits context-dependent roles in cancer; it acts as a tumor suppressor in PTEN-deficient glioblastoma by attenuating AKT signaling, whereas it is required for the maintenance of leukemia-initiating cells in acute myeloid leukemia. Its loss in leukemic contexts triggers cell-cycle arrest, highlighting its potential as a therapeutic target in specific hematological malignancies.