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      Four pairs of gene–gene interactions associated with increased risk for type 2 diabetes (CDKN2BAS–KCNJ11), obesity (SLC2A9–IGF2BP2, FTO–APOA5), and hypertension (MC4R–IGF2BP2) in Chinese women

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          Abstract

          Metabolic disorders including type 2 diabetes, obesity and hypertension have growing prevalence globally every year. Genome-wide association studies have successfully identified many genetic markers associated to these diseases, but few studied their interaction effects. In this study, twenty candidate SNPs from sixteen genes are selected, and a lasso-multiple regression approach is implemented to consider the SNP–SNP interactions among them in an Asian population. It is found out that the main effects of the markers are weak but the interactions among the candidates showed a significant association to diseases. SNPs from genes CDKN2BAS and KCNJ11 are significantly associated to risk for developing diabetes, and SNPs from FTO and APOA5 might interact to play an important role for the onset of hypertension.

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          The Adaptive Lasso and Its Oracle Properties

          Hui Zou (2006)
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            The obesity-associated FTO gene encodes a 2-oxoglutarate-dependent nucleic acid demethylase.

            Thomas Gerken, Christophe A Girard, Yi-Chun Loraine Tung … (2007)
            Variants in the FTO (fat mass and obesity associated) gene are associated with increased body mass index in humans. Here, we show by bioinformatics analysis that FTO shares sequence motifs with Fe(II)- and 2-oxoglutarate-dependent oxygenases. We find that recombinant murine Fto catalyzes the Fe(II)- and 2OG-dependent demethylation of 3-methylthymine in single-stranded DNA, with concomitant production of succinate, formaldehyde, and carbon dioxide. Consistent with a potential role in nucleic acid demethylation, Fto localizes to the nucleus in transfected cells. Studies of wild-type mice indicate that Fto messenger RNA (mRNA) is most abundant in the brain, particularly in hypothalamic nuclei governing energy balance, and that Fto mRNA levels in the arcuate nucleus are regulated by feeding and fasting. Studies can now be directed toward determining the physiologically relevant FTO substrate and how nucleic acid methylation status is linked to increased fat mass.
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              Molecular interplay of the noncoding RNA ANRIL and methylated histone H3 lysine 27 by polycomb CBX7 in transcriptional silencing of INK4a.

              Kyoko Yap, Side Li, Ana Muñoz-Cabello … (2010)
              Expression of the INK4b/ARF/INK4a tumor suppressor locus in normal and cancerous cell growth is controlled by methylation of histone H3 at lysine 27 (H3K27me) as directed by the Polycomb group proteins. The antisense noncoding RNA ANRIL of the INK4b/ARF/INK4a locus is also important for expression of the protein-coding genes in cis, but its mechanism has remained elusive. Here we report that chromobox 7 (CBX7) within the polycomb repressive complex 1 binds to ANRIL, and both CBX7 and ANRIL are found at elevated levels in prostate cancer tissues. In concert with H3K27me recognition, binding to RNA contributes to CBX7 function, and disruption of either interaction impacts the ability of CBX7 to repress the INK4b/ARF/INK4a locus and control senescence. Structure-guided analysis reveals the molecular interplay between noncoding RNA and H3K27me as mediated by the conserved chromodomain. Our study suggests a mechanism by which noncoding RNA participates directly in epigenetic transcriptional repression. Copyright (c) 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                M.M.Y. Waye
                Journal
                Journal ID (nlm-ta): Meta Gene
                Journal ID (iso-abbrev): Meta Gene
                Title: Meta Gene
                Publisher: Elsevier
                ISSN (Electronic): 2214-5400
                Publication date PMC-release: 21 May 2014
                Publication date Collection: December 2014
                Publication date (Electronic): 21 May 2014
                Volume: 2
                Pages: 384-391
                Affiliations
                [a ]Division of Biostatistics, School of Public Health and Primary Care, The Chinese University of Hong Kong, Shatin, Hong Kong Special Administrative Region
                [b ]School of Life Sciences, The Chinese University of Hong Kong, Shatin, Hong Kong Special Administrative Region
                [c ]School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, Hong Kong Special Administrative Region
                [d ]Division of Epidemiology, School of Public Health and Primary Care, The Chinese University of Hong Kong, Shatin, Hong Kong Special Administrative Region
                Author notes
                [* ]Corresponding author. Tel.: + 852 3943 6874; fax: + 852 2603 5123. mary-waye@ 123456cuhk.edu.hk
                [1]

                First authors.

                Article
                Publisher ID: S2214-5400(14)00029-2
                DOI: 10.1016/j.mgene.2014.04.010
                PMC ID: 4287808
                PubMed ID: 25606423
                SO-VID: 23031a1f-6782-418d-9c21-5d0dfdf4dac3
                Copyright © © 2014 The Authors. Published by Elsevier B.V.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).

                History
                Date received : 4 December 2013
                Date revision received : 1 April 2014
                Date accepted : 25 April 2014
                Categories
                Subject: Article

                Keywords: metabolic disorder,candidate genes,interaction effects
                Data availability:
                Keywords: metabolic disorder, candidate genes, interaction effects

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