ArticleExperimental diabetes research2011
Frequent loss of genome gap region in 4p16.3 subtelomere in early-onset type 2 diabetes mellitus.
Article in Experimental diabetes research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Simultaneous copy number losses within multiple subtelomeric regions in early-onset type 2 diabetes mellitus.PloS one · 2014Trial
- Contribution of rare variants to heritability of a disease is much greater than conventionally estimated: modification of allele distribution model.Journal of human genetics · 2024Article
- Clinical and genetic analysis in a Chinese cohort of children and adolescents with diabetes/persistent hyperglycemia.Journal of diabetes investigation · 2021Article
- Copy number loss in the region of theBone & joint research · 2017Article
- Copy number variations play important roles in heredity of common diseases: a novel method to calculate heritability of a polymorphism.Scientific reports · 2015Article
- The evolution of African great ape subtelomeric heterochromatin and the fusion of human chromosome 2.Genome research · 2012Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A small portion of Type 2 diabetes mellitus (T2DM) is familial, but the majority occurs as sporadic disease. Although causative genes are found in some rare forms, the genetic basis for sporadic T2DM is largely unknown. We searched for a copy number abnormality in 100 early-onset Japanese T2DM patients (onset age <35 years) by whole-genome screening with a copy number variation BeadChip. Within the 1.3-Mb subtelomeric region on chromosome 4p16.3, we found copy number losses in early-onset T2DM (13 of 100 T2DM versus one of 100 controls). This region surrounds a genome gap, which is rich in multiple low copy repeats. Subsequent region-targeted high-density custom-made oligonucleotide microarray experiments verified the copy number losses and delineated structural changes in the 1.3-Mb region. The results suggested that copy number losses of the genes in the deleted region around the genome gap in 4p16.3 may play significant roles in the etiology of T2DM.
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