ArticleScientific reports2020
Genomic imprinting analyses identify maternal effects as a cause of phenotypic variability in type 1 diabetes and rheumatoid arthritis.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Relative maternal protection against type 1 diabetes: A combined analysis of 5 observational studies.The Journal of clinical endocrinology and metabolism · 2026Article
- DNA Methylation NearPediatric diabetes · 2023Article
- Epigenome association study for DNA methylation biomarkers in buccal and monocyte cells for female rheumatoid arthritis.Scientific reports · 2021Article
- Astragaloside regulates lncRNA LOC100912373 and the miR‑17‑5p/PDK1 axis to inhibit the proliferation of fibroblast‑like synoviocytes in rats with rheumatoid arthritis.International journal of molecular medicine · 2021Article
- Epigenetic Changes Induced by Maternal Factors during Fetal Life: Implication for Type 1 Diabetes.Genes · 2021Review
- Epigenetic Contribution and Genomic Imprinting Dlk1-Dio3 miRNAs in Systemic Lupus Erythematosus.Genes · 2021Review
- Imprinted Genes and Multiple Sclerosis: What Do We Know?International journal of molecular sciences · 2021Review
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Authors and funding
8 authors.
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Abstract
Imprinted genes, giving rise to parent-of-origin effects (POEs), have been hypothesised to affect type 1 diabetes (T1D) and rheumatoid arthritis (RA). However, maternal effects may also play a role. By using a mixed model that is able to simultaneously consider all kinds of POEs, the importance of POEs for the development of T1D and RA was investigated in a variance components analysis. The analysis was based on Swedish population-scale pedigree data. With P = 0.18 (T1D) and P = 0.26 (RA) imprinting variances were not significant. Explaining up to 19.00% (± 2.00%) and 15.00% (± 6.00%) of the phenotypic variance, the maternal environmental variance was significant for T1D (P = 1.60 × 10
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