人 PIP4K2B 抗体对
01AB02520
Phosphatidylinositol-5-phosphate 4-kinase type 2 beta (PIP4K2B) is a nuclear-enriched lipid kinase that phosphorylates phosphatidylinositol-5-phosphate (PI5P) to generate phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2). It functions as a critical regulator of nuclear lipid messenger homeostasis and acts as a GTP sensor for metabolic adaptation. PIP4K2B modulates insulin signaling by interacting with PIP5Ks to control the production of downstream phosphoinositides. Additionally, it is mechanoresponsive, influencing nuclear envelope tension, heterochromatin organization via UHRF1, and YAP localization. Clinically, mutations in PIP4K2B are linked to myeloid cell homeostasis disorders, including severe congenital neutropenia 7 and hereditary neutrophilia. Its role in regulating cellular mechanics and signaling suggests broader implications in metabolic and oncogenic processes.
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技术参数
- 靶点基因名
- PIP4K2B
- 基因别名
- PIP5K2B
- 蛋白别名
- phosphatidylinositol-5-phosphate 4-kinase type 2 beta; PIP4K2B
- UniProt
- P78356
- 物种
- Human
产品详情
- 靶点名称
- PIP4K2B
- 蛋白名称
- phosphatidylinositol-5-phosphate 4-kinase type 2 beta
- 蛋白别名
- Phosphatidylinositol 5-phosphate 4-kinase type-2 beta; 1-phosphatidylinositol 5-phosphate 4-kinase 2-beta; Diphosphoinositide kinase 2-beta; Phosphatidylinositol 5-phosphate 4-kinase type II beta; PI(5)P 4-kinase type II beta; PIP4KII-beta; PtdIns(5)P-4-kinase isoform 2-beta
- 靶点基因名
- PIP4K2B
- 基因别名
- PIP5K2B
- UniProt
- P78356
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Phosphatidylinositol-5-phosphate 4-kinase type 2 beta (PIP4K2B) is a nuclear-enriched lipid kinase that phosphorylates phosphatidylinositol-5-phosphate (PI5P) to generate phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2). It functions as a critical regulator of nuclear lipid messenger homeostasis and acts as a GTP sensor for metabolic adaptation. PIP4K2B modulates insulin signaling by interacting with PIP5Ks to control the production of downstream phosphoinositides. Additionally, it is mechanoresponsive, influencing nuclear envelope tension, heterochromatin organization via UHRF1, and YAP localization. Clinically, mutations in PIP4K2B are linked to myeloid cell homeostasis disorders, including severe congenital neutropenia 7 and hereditary neutrophilia. Its role in regulating cellular mechanics and signaling suggests broader implications in metabolic and oncogenic processes.