Target intelligence / Profile preview

Phosphatidylinositol-4-phosphate 5-kinase type 1 beta (PIP5K1B)

Target
PIP5K1B
Molecular classification
Enzyme, Kinase
01

Overview

Phosphatidylinositol-4-phosphate 5-kinase type 1 beta (PIP5K1B) is an enzyme that catalyzes the phosphorylation of phosphatidylinositol 4-phosphate (PI4P) to generate phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), a key lipid second messenger involved in the regulation of signal transduction, cytoskeleton remodeling, vesicle trafficking, cell adhesion, and motility[1][2][8]. PI(4,5)P2 directly acts as a second messenger or serves as a precursor for the production of inositol 1,4,5-trisphosphate (IP3), diacylglycerol (DAG), and phosphatidylinositol 3,4,5-trisphosphate (PIP3)[1][8]. PIP5K1B activity is implicated in the regulation of actin cytoskeleton through RAC1-mediated pathways and in platelet adhesion following GPCR stimulation[1]. Genetic or epigenetic silencing of PIP5K1B is associated with cytoskeletal defects observed in Friedreich ataxia, and aberrant PIP5K1B signaling is linked to oncogenic PI3K pathway activation in cancer[1][2][4].

Other names
MSS4STM7PIP5K1-betaPIP5KIbetaphosphatidylinositol 4-phosphate 5-kinase type I betaprotein STM-7type I phosphatidylinositol 4-phosphate 5-kinase betaPI51BPI4P5K-IbPipk5btype I PIP kinase beta
02

Mechanism of action

Inhibition or modulation of kinase enzymatic activity to alter levels of phosphoinositide lipids (no approved drugs or clinical candidates known)

03

Biological functions

Phosphatidylinositol phosphate biosynthesisSignal transductionRegulation of actin cytoskeleton dynamicsVesicle traffickingCell adhesionCell motility
04

Disease associations

Friedreich ataxiaCancer (via PI3K pathway, support for role in oncogenic signaling)Other (impaired cytoskeletal dynamics in neurodegeneration)
05

Safety considerations

Potential for widespread cellular effects due to role in fundamental signaling pathways, actin dynamics, and vesicle trafficking; specific concerns not documented, but disruptions could impact multiple cell types[1][2][8]

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