ArticleDiabetologia2016
Excess maternal transmission of variants in the THADA gene to offspring with type 2 diabetes.
Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Pooled it
- Article
- THADA inhibits autophagy and increases 5-FU sensitivity in gastric cancer cells via the PI3K/AKT/mTOR signaling pathway.Iranian journal of basic medical sciences · 2024Article
- The value of parental medical records for the prediction of diabetes and cardiovascular disease: a novel method for generating and incorporating family histories.Journal of the American Medical Informatics Association : JAMIA · 2023Article
- THADA inhibition in mice protects against type 2 diabetes mellitus by improving pancreatic β-cell function and preserving β-cell mass.Nature communications · 2023Article
- Article
- THADA drives Golgi residency and upregulation of PD-L1 in cancer cells and provides promising target for immunotherapy.Journal for immunotherapy of cancer · 2021Article
- Copy number variations in candidate genomic regions confirm genetic heterogeneity and parental bias in Hirschsprung disease.Orphanet journal of rare diseases · 2019Article
- Review
- Haplotype Sharing Provides Insights into Fine-Scale Population History and Disease in Finland.American journal of human genetics · 2018Article
- Maternal transmission disequilibrium of rs2248359 in type 2 diabetes mellitus families and its association with vitamin D level in offspring.Scientific reports · 2018Article
- New approaches beyond genetics: towards precision medicine in diabetes.Diabetologia · 2016Article
Corrections and comments
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Authors and funding
21 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisGenome-wide association studies (GWAS) have identified more than 65 genetic loci associated with risk of type 2 diabetes. However, the contribution of distorted parental transmission of alleles to risk of type 2 diabetes has been mostly unexplored. Our goal was therefore to search for parent-of-origin effects (POE) among type 2 diabetes loci in families.
methodsFamilies from the Botnia study (n = 4,211, 1,083 families) were genotyped for 72 single-nucleotide polymorphisms (SNPs) associated with type 2 diabetes and assessed for POE on type 2 diabetes. The family-based Hungarian Transdanubian Biobank (HTB) (n = 1,463, >135 families) was used to replicate SNPs showing POE. Association of type 2 diabetes loci within families was also tested.
resultsThree loci showed nominal POE, including the previously reported variants in KCNQ1, for type 2 diabetes in families from Botnia (rs2237895: p POE = 0.037), which can be considered positive controls. The strongest POE was seen for rs7578597 SNP in the THADA gene, showing excess transmission of the maternal risk allele T to diabetic offspring (Botnia: p POE = 0.01; HTB p POE = 0.045). These data are consistent with previous evidence of allelic imbalance for expression in islets, suggesting that the THADA gene can be imprinted in a POE-specific fashion. Five CpG sites, including those flanking rs7578597, showed differential methylation between diabetic and non-diabetic donor islets. CONCLUSIONS/
interpretationTaken together, the data emphasise the need for genetic studies to consider from which parent an offspring has inherited a susceptibility allele.
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