ArticleAnnals of human genetics2014
ABCC5 transporter is a novel type 2 diabetes susceptibility gene in European and African American populations.
Article in Annals of human genetics, 2014. 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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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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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- An Emerging Paradigm for ABCC5/MRP5 Function in Human Physiology.International journal of molecular sciences · 2025Review
- The murine ATP-binding cassette transporter C5 (Abcc5/MRP5/cMOAT) plays a role in memory consolidation, circadian rhythm regulation and glutamatergic signalling.Translational psychiatry · 2025Article
- Decoding cardiovascular risks: analyzing type 2 diabetes mellitus and ASCVD gene expression.Frontiers in endocrinology · 2024Article
- New Insights Into Mitochondrial Dysfunction at Disease Susceptibility Loci in the Development of Type 2 Diabetes.Frontiers in endocrinology · 2021Article
- Updates on Genes and Genetic Mechanisms Implicated in Primary Angle-Closure Glaucoma.The application of clinical genetics · 2021Review
- Abcc5 Knockout Mice Have Lower Fat Mass and Increased Levels of Circulating GLP-1.Obesity (Silver Spring, Md.) · 2019Article
- High-Resolution Genetic Maps Identify Multiple Type 2 Diabetes Loci at Regulatory Hotspots in African Americans and Europeans.American journal of human genetics · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Numerous functional studies have implicated PARL in relation to type 2 diabetes (T2D). We hypothesised that conflicting human association studies may be due to neighbouring causal variants being in linkage disequilibrium (LD) with PARL. We conducted a comprehensive candidate gene study of the extended LD genomic region that includes PARL and transporter ABCC5 using three data sets (two European and one African American), in relation to healthy glycaemic variation, visceral fat accumulation and T2D disease. We observed no evidence for previously reported T2D association with Val262Leu or PARL using array and fine-map genomic and expression data. By contrast, we observed strong evidence of T2D association with ABCC5 (intron 26) for European and African American samples (P = 3E-07) and with ABCC5 adipose expression in Europeans [odds ratio (OR) = 3.8, P = 2E-04]. The genomic location estimate for the ABCC5 functional variant, associated with all phenotypes and expression data (P = 1E-11), was identical for all samples (at Chr3q 185,136 kb B36), indicating that the risk variant is an expression quantitative trait locus (eQTL) with increased expression conferring risk of disease. That the association with T2D is observed in populations of disparate ancestry suggests the variant is a ubiquitous risk factor for T2D.
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Registered trials
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