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Inositol 1,4,5-trisphosphate 3-kinase C (ITPKC)
- Target
- ITPKC
- Molecular classification
- Enzyme, Kinase, Transferase
01
Overview
Inositol 1,4,5-trisphosphate 3-kinase C (ITPKC) is one of three ITP3K isoforms in mammals, functioning as an enzyme that phosphorylates inositol 1,4,5-trisphosphate (IP₃) to inositol 1,3,4,5-tetrakisphosphate (IP₄), thus terminating IP₃-dependent calcium release from the endoplasmic reticulum. ITPKC regulates the intensity and duration of calcium signaling cascades, impacting diverse processes such as cell signaling, immune cell maturation, and neuronal synaptic plasticity. Genetic variations in ITPKC have clinical relevance in Kawasaki disease, an inflammatory illness with potential for serious cardiac complications.
- Other names
- ITP3KCIP3KCinositol-trisphosphate 3-kinase Cinositol 1,4,5-trisphosphate 3-kinase C
02
Mechanism of action
Not directly drug-targeted; the mechanism of action would involve: Inhibition or modulation of ITPKC enzymatic activity would alter phosphorylation of inositol 1,4,5-trisphosphate, thus affecting termination of Ca²⁺ signaling and subsequent downstream events
03
Biological functions
Signal transductionRegulation of intracellular calcium levelsTermination of inositol phosphate-mediated Ca²⁺ signalingCytoskeletal regulation (actin microstructure modulation)Modulation of immune cell activation and neuronal plasticity
04
Disease associations
Genetic susceptibility to Kawasaki diseaseHeart aneurysm riskInvolvement in immune function abnormalitiesPossible roles in neuronal disorders due to regulation of neuronal signaling
05
Safety considerations
Given the enzyme’s critical role in immune signaling and calcium homeostasis, inhibition or dysregulation could cause immune dysfunction, impaired calcium signaling, or cardiovascular issues
06
Biomarkers
Genotype (polymorphisms) of the ITPKC gene can serve as a biomarker for risk of Kawasaki disease and associated cardiac complications
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