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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Inositol-trisphosphate 3-kinase C

ITPKC, inositol 1,4,5-trisphosphate 3-kinase C, IP3K-C, Inositol trisphosphate 3-kinase C
This gene encodes a member of the inositol 1,4,5-trisphosphate [Ins(1,4,5)P(3)] 3-kinase family of enzymes that catalyze the phosphorylation of inositol 1,4,5-trisphosphate to 1,3,4,5-tetrakisphosphate. The encoded protein is localized to the nucleus and cytoplasm and has both nuclear import and nuclear export activity. Single nucleotide polymorphisms in this gene are associated with Kawasaki disease.[provided by RefSeq, Sep 2009] (from NCBI)
Top mentioned proteins: CAN, HAD, Itpkb, inositol 1,4,5-trisphosphate 3-kinase, AGE
Papers on ITPKC
Regulation of NGF-driven neurite outgrowth by Ins(1,4,5)P3 kinase is specifically associated with the two isoenzymes Itpka and Itpkb in a model of PC12 cells.
Erneux et al., Brussels, Belgium. In Febs J, Jul 2015
Four inositol phosphate kinases catalyze phosphorylation of the second messenger inositol 1,4,5-trisphosphate [Ins(1,4,5)P3 ] to inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P4 ]: these enzymes comprise three isoenzymes of inositol 1,4,5-trisphosphate 3-kinase (Itpk), referred to as Itpka, Itpkb and Itpkc, and the inositol polyphosphate multikinase (IPMK).
Update of genetic susceptibility in patients with Kawasaki disease.
Yoon, Seoul, South Korea. In Korean J Pediatr, Mar 2015
This review revealed numerous potential susceptibility genes including genetic polymorphisms of ITPKC, CASP3, the transforming growth factor-β signaling pathway, B lymphoid tyrosine kinase, FCGR2A, KCNN2, and other genes, an imbalance of Th17/Treg, and a range of suggested future treatment options.
Intravenous immunoglobulin, pharmacogenomics, and Kawasaki disease.
Chang et al., Kao-hsiung, Taiwan. In J Microbiol Immunol Infect, 2014
Findings in the past decade have contributed to a major breakthrough in the genetics of KD, with the identification of several genomic regions linked to the pathogenesis of KD, including ITPKC, CD40, BLK, and FCGR2A.
[Cyclosporin A treatment for refractory Kawasaki disease].
Shibuta et al., In Nihon Rinsho, 2014
The association between functional polymorphism of inositol 1,4,5-trisphosphate 3- kinase-C(ITPKC) and susceptibility to Kawasaki disease(KD) and formation of coronary arterial lesions was reported in 2008.
Management of Kawasaki disease.
Brogan et al., London, United Kingdom. In Arch Dis Child, 2014
Genetic studies have identified several susceptibility genes for KD and its sequelae in different ethnic populations, including FCGR2A, CD40, ITPKC, FAM167A-BLK and CASP3, as well as genes influencing response to intravenous immunoglobulin (IVIG) and aneurysm formation such as FCGR3B, and transforming growth factor (TGF) β pathway genes.
Study of the association between ITPKC genetic polymorphisms and calcium nephrolithiasis.
Chang et al., Tainan City, Taiwan. In Biomed Res Int, 2013
Inositol 1,4,5-trisphosphate (IP3) 3-kinase C (ITPKC) is a negative regulator of the SOC channel-mediated signaling pathway.
Single-nucleotide polymorphism rs7251246 in ITPKC is associated with susceptibility and coronary artery lesions in Kawasaki disease.
Chang et al., Kao-hsiung, Taiwan. In Plos One, 2013
A single nucleotide polymorphism (SNP) in inositol 1,4,5-trisphosphate 3-kinase C (ITPKC) has been identified to be an important polymorphism in the risk of KD.
Identification of hepatic microvascular adhesion-related genes of human colon cancer cells using random homozygous gene perturbation.
Vidal-Vanaclocha et al., Leioa, Spain. In Int J Cancer, 2013
Others were antiadhesive genes detected because of their overexpression in nonadherent HT-29 cells (ITPKC gene) and their silenced status in adherent HT-29 cells (PPP6R2 gene).
Mercury promotes catecholamines which potentiate mercurial autoimmunity and vasodilation: implications for inositol 1,4,5-triphosphate 3-kinase C susceptibility in kawasaki syndrome.
Kuo et al., Shawnee, United States. In Korean Circ J, 2013
Previously, we reviewed biological evidence that mercury could induce autoimmunity and coronary arterial wall relaxation as observed in Kawasaki syndrome (KS) through its effects on calcium signaling, and that inositol 1,4,5-triphosphate 3-kinase C (ITPKC) susceptibility in KS would predispose patients to mercury by increasing Ca(2+) release.
Superantigen involvement and susceptibility factors in Kawasaki disease: profiles of TCR Vβ2+ T cells and HLA-DRB1, TNF-α and ITPKC genes among Filipino patients.
Saloma et al., Quezon, Philippines. In Int J Mol Epidemiol Genet, 2012
To investigate these roles, percentages of TCR-Vβ2+ T cells were compared by flow cytometry using anti-Vβ2 monoclonal antibodies and genotyping was done on HLA-DRB1 exon 2, the -308 site of the TNF-α promoter region, and ITPKC SNP rs28493229 by polymerase chain reaction followed by direct sequencing.
A replication study for association of ITPKC and CASP3 two-locus analysis in IVIG unresponsiveness and coronary artery lesion in Kawasaki disease.
Chang et al., Kao-hsiung, Taiwan. In Plos One, 2012
Single-nucleotide polymorphisms (SNPs) in inositol 1,4,5-trisphosphate 3-kinase C (ITPKC, rs28493229) and caspase-3 (CASP3, rs113420705) are associated with susceptibility to KD in Japanese and Taiwanese populations.
PPP3CC feedback regulates IP3-Ca2+ pathway through preventing ITPKC degradation.
Huo et al., Shanghai, China. In Front Biosci, 2012
ITPKC, a susceptibility gene of Kawasaki disease, encodes a kinase that negatively regulates intracellular Ca2+ level and inhibits calcineurin-dependent activation of NFAT by phosphorylating IP3.
ITPKC susceptibility in Kawasaki syndrome as a sensitizing factor for autoimmunity and coronary arterial wall relaxation induced by thimerosal's effects on calcium signaling via IP3.
Deth et al., Shawnee, United States. In Autoimmun Rev, 2012
Recently, a single nucleotide polymorphism (SNP) of the inositol 1,4,5-triphosphate kinase C (ITPKC), rs28493229, was found to passively confer susceptibility for Kawasaki syndrome (KS) and subsequent coronary arterial lesions.
Genome-wide association study identifies FCGR2A as a susceptibility locus for Kawasaki disease.
Blue Mountains Eye Study et al., Singapore, Singapore. In Nat Genet, 2011
The second locus is at 19q13, (P = 2.51 × 10(-9), OR = 1.42 for the rs2233152 SNP near MIA and RAB4B; P = 1.68 × 10(-12), OR = 1.52 for rs28493229 in ITPKC), which confirms previous findings(1).
[Association study of a functional SNP rs28493229 of ITPKC gene and Kawasaki disease in a Chinese population].
Zhang et al., Chengdu, China. In Zhonghua Yi Xue Yi Chuan Xue Za Zhi, 2011
The study failed to prove any association between SNP rs28493229 of ITPKC gene and Kawasaki disease/coronary artery lesions in Chinese patients.
Clinical Implication of the C Allele of the ITPKC Gene SNP rs28493229 in Kawasaki Disease: Association With Disease Susceptibility and BCG Scar Reactivation.
Wu et al., Taipei, Taiwan. In Pediatr Infect Dis J, 2011
Single nucleotide polymorphism rs28493229 in ITPKC contributes to Kawasaki disease susceptibility through induced hyperimmune function reflected in the BCG reactivation.
ITPKC single nucleotide polymorphism associated with the Kawasaki disease in a Taiwanese population.
Chang et al., Kao-hsiung, Taiwan. In Plos One, 2010
results indicated that C-allele of ITPKC SNP rs28493229 is associated with the susceptibility and aneurysm formation in KD patients in a Taiwanese population
ITPKC gene SNP rs28493229 and Kawasaki disease in Taiwanese children.
Lee et al., Taipei, Taiwan. In Hum Mol Genet, 2010
A statistically significant association was not found between the ITPKC gene single-nucleotide polymorphism rs28493229 and Kawasaki disease or coronary artery lesions in Taiwanese children.
ITPKC functional polymorphism associated with Kawasaki disease susceptibility and formation of coronary artery aneurysms.
Hata et al., Yokohama, Japan. In Nat Genet, 2008
ITPKC acts as a negative regulator of T-cell activation through the Ca2+/NFAT signaling pathway, and the C allele may contribute to immune hyper-reactivity in Kawasaki disease.
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