ArticleNature communications2025
Genetics of circulating proteins in newborn babies at high risk of type 1 diabetes.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Familial and genetic overlap between Sjögren's disease and other autoimmune diseases.Frontiers in immunology · 2026Pooled it
- Clinical Utility of a Type 1 Diabetes Genetic Risk Score Measured as Part of MODY Genetic Testing.Diabetes care · 2026Article
- Development and Validation of a Streamlined Workflow for Proteomic Analysis of Proteins and Post-translational Modifications from Dried Blood.Journal of proteome research · 2026Article
- Article
- Development and validation of a streamlined workflow for proteomic analysis of proteins and post-translational modifications from dried blood.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
21 authors.
Funding
Abstract
Type 1 diabetes is a chronic, autoimmune disease characterized by the destruction of insulin-producing β-cells in the pancreas. Early detection can facilitate timely intervention, potentially delaying or preventing disease onset. Circulating proteins reflect dysregulated biological processes and offer insights into early disease mechanisms. Here, we construct a genome-wide pQTL map of 1985 proteins in 695 newborn babies (median age 2 days) at increased genetic risk of developing Type 1 diabetes. We identify 535 pQTLs (352 cis-pQTLs, 183 trans-pQTLs), 62 of which characteristic of newborns. We show colocalization of pQTLs for CTRB1, APOBR, IL7R, CPA1, and PNLIPRP1 with Type 1 diabetes GWAS signals, and Mendelian randomization causally implicates each of these five proteins in the aetiology of Type 1 diabetes. Our study illustrates the utility of newborn molecular profiles for discovering potential drug targets for childhood diseases of significant concern.
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Registered trials
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