ArticlePloS one2015
Fine Mapping of a GWAS-Derived Obesity Candidate Region on Chromosome 16p11.2.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.
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Who cites it
8 citing papers in PubMed, 2 syntheses or guidelines pooled it, 13 citations in OpenAlex.
- Identifying BMI-associated genes via a genome-wide multi-omics integrative approach using summary data.Human molecular genetics · 2024Pooled it
- A Genomewide Integrative Analysis of GWAS and eQTLs Data Identifies Multiple Genes and Gene Sets Associated with Obesity.BioMed research international · 2018Pooled it
- Genome-wide association study of delay discounting identifies 11 loci and reveals transdiagnostic associations across mental and physical health.Molecular psychiatry · 2026Article
- Loss of Sult1a1 reduces body weight and increases browning of white adipose tissue.Frontiers in endocrinology · 2024Article
- Genetic impacts on DNA methylation help elucidate regulatory genomic processes.Genome biology · 2023Article
- Association of SULT1A2 rs1059491 with obesity and dyslipidaemia in southern Chinese adults.Scientific reports · 2023Article
- The Role of Genetic Variation of BMI, Body Composition, and Fat Distribution for Mental Traits and Disorders: A Look-Up and Mendelian Randomization Study.Frontiers in genetics · 2020Article
- The Effect of SH2B1 Variants on Expression of Leptin- and Insulin-Induced Pathways in Murine Hypothalamus.Obesity facts · 2018Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionLarge-scale genome-wide association studies (GWASs) have identified 97 chromosomal loci associated with increased body mass index in population-based studies on adults. One of these SNPs, rs7359397, tags a large region (approx. 1MB) with high linkage disequilibrium (r2>0.7), which comprises five genes (SH2B1, APOBR, sulfotransferases: SULT1A1 and SULT1A2, TUFM). We had previously described a rare mutation in SH2B1 solely identified in extremely obese individuals but not in lean controls.
methodsThe coding regions of the genes APOBR, SULT1A1, SULT1A2, and TUFM were screened for mutations (dHPLC, SSCP, Sanger re-sequencing) in 95 extremely obese children and adolescents. Detected non-synonymous variants were genotyped (TaqMan SNP Genotyping, MALDI TOF, PCR-RFLP) in independent large study groups (up to 3,210 extremely obese/overweight cases, 485 lean controls and 615 obesity trios). In silico tools were used for the prediction of potential functional effects of detected variants.
resultsExcept for TUFM we detected non-synonymous variants in all screened genes. Two polymorphisms rs180743 (APOBR p.Pro428Ala) and rs3833080 (APOBR p.Gly369_Asp370del9) showed nominal association to (extreme) obesity (uncorrected p = 0.003 and p = 0.002, respectively). In silico analyses predicted a functional implication for rs180743 (APOBR p.Pro428Ala). Both APOBR variants are located in the repetitive region with unknown function.
conclusionVariants in APOBR contributed as strongly as variants in SH2B1 to the association with extreme obesity in the chromosomal region chr16p11.2. In silico analyses implied no functional effect of several of the detected variants. Further in vitro or in vivo analyses on the functional implications of the obesity associated variants are warranted.
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