SynthesisMolecular biology reports2012
A functional polymorphism, rs28493229, in ITPKC and risk of Kawasaki disease: an integrated meta-analysis.
Synthesis in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.
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The trial behind it
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Who cites it
20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.
- A comprehensive integration of data on the association of ITPKC polymorphisms with susceptibility to Kawasaki disease: a meta-analysis.BMC medical genomics · 2025Pooled it
- Association of ITPKC gene polymorphisms rs28493229 and rs2290692 in North Indian children with Kawasaki disease.Pediatric research · 2022Pooled it
- Rationale and study design for a phase I/IIa trial of anakinra in children with Kawasaki disease and early coronary artery abnormalities (the ANAKID trial).Contemporary clinical trials · 2016Trial
- Article
- Immunogenetics of Kawasaki disease.Clinical reviews in allergy & immunology · 2020Review
- Blood Mercury Levels in Children with Kawasaki Disease and Disease Outcome.International journal of environmental research and public health · 2020Article
- The role of CaScientific reports · 2020Article
- Lower CMV and EBV Exposure in Children With Kawasaki Disease Suggests an Under-Challenged Immune System.Frontiers in pediatrics · 2020Article
- Antibodies and Immunity During Kawasaki Disease.Frontiers in cardiovascular medicine · 2020Review
- Dissecting Kawasaki disease: a state-of-the-art review.European journal of pediatrics · 2017Review
- Potential association between ITPKC genetic variations and Hirschsprung disease.Molecular biology reports · 2017Article
- Review: Found in Translation: International Initiatives Pursuing Interleukin-1 Blockade for Treatment of Acute Kawasaki Disease.Arthritis & rheumatology (Hoboken, N.J.) · 2017Review
- Genetic variants of ADAM17 are implicated in the pathological process of Kawasaki disease and secondary coronary artery lesions via the TGF-β/SMAD3 signaling pathway.European journal of pediatrics · 2016Article
- Ethnic Kawasaki Disease Risk Associated with Blood Mercury and Cadmium in U.S. Children.International journal of environmental research and public health · 2016Article
- Article
- IL-1 Signaling Is Critically Required in Stromal Cells in Kawasaki Disease Vasculitis Mouse Model: Role of Both IL-1α and IL-1β.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Systematic confirmation study of GWAS-identified genetic variants for Kawasaki disease in a Chinese population.Scientific reports · 2015Article
- The roles of Ca2+/NFAT signaling genes in Kawasaki disease: single- and multiple-risk genetic variants.Scientific reports · 2014Article
- Single-nucleotide polymorphism rs7251246 in ITPKC is associated with susceptibility and coronary artery lesions in Kawasaki disease.PloS one · 2014Article
- Mercury promotes catecholamines which potentiate mercurial autoimmunity and vasodilation: implications for inositol 1,4,5-triphosphate 3-kinase C susceptibility in kawasaki syndrome.Korean circulation journal · 2013Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kawasaki disease (KD) is a multi-systemic vasculitis which preferentially affects infants and children. A single nucleotide polymorphism (rs28493229) in the inositol 1,4,5-trisphosphate 3-kinase C (ITPKC) was identified to be associated with the increased risk of KD; however, in more recent studies associations have been controversial. Thus, we performed a meta-analysis, integrating case-control and transmission/disequilibrium test (TDT) studies, to investigate the relationship between this polymorphism and risk of KD. A total of ten case-control and two TDT studies, comprising 3,821 cases, 12,802 controls and 949 families, were included in this meta-analysis. There was a significant association between the C allele of rs28493229 and the increased risk of KD (OR = 1.53, 95 % CI = 1.34-1.74, P < 0.001), by the random-effects model because of heterogeneity (Q = 27.67, P (heterogeneity) = 0.004). Nevertheless, it was screened out by meta-regression analysis that the coronary artery lesions (CALs) status of KD could partly explain the heterogeneity, with consistently significant associations in both subgroups after stratification by CALs status. Moreover, estimates before and after the deletion of each study were similar in sensitivity analysis, indicating robust stability of the meta-analysis. This meta-analysis reveals that the functional polymorphism rs28493229 in ITPKC significantly contributes to the risk of KD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.