Fine mapping of type 1 diabetes susceptibility loci and evidence for colocalization of causal variants with lymphoid gene enhancers

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F15%3A10294671" target="_blank" >RIV/00216208:11130/15:10294671 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00064203:_____/15:10294671

Výsledek na webu

<a href="http://dx.doi.org/10.1038/ng.3245" target="_blank" >http://dx.doi.org/10.1038/ng.3245</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/ng.3245" target="_blank" >10.1038/ng.3245</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Fine mapping of type 1 diabetes susceptibility loci and evidence for colocalization of causal variants with lymphoid gene enhancers

Popis výsledku v původním jazyce

Genetic studies of type 1 diabetes (T1D) have identified 50 susceptibility regions(1,2), finding major pathways contributing to risk(3), with some loci shared across immune disorders(4-6). To make genetic comparisons across autoimmune disorders as informative as possible, a dense genotyping array, the Immunochip, was developed, from which we identified four new T1D-associated regions (P < 5 x 10(-8)). A comparative analysis with 15 immune diseases showed that T1D is more similar genetically to other autoantibody-positive diseases, significantly most similar to juvenile idiopathic arthritis and significantly least similar to ulcerative colitis, and provided support for three additional new T1D risk loci. Using a Bayesian approach, we defined credible sets for the T1D-associated SNPs. The associated SNPs localized to enhancer sequences active in thymus, T and B cells, and CD34(+) stem cells. Enhancer-promoter interactions can now be analyzed in these cell types to identify which particul

Název v anglickém jazyce

Fine mapping of type 1 diabetes susceptibility loci and evidence for colocalization of causal variants with lymphoid gene enhancers

Popis výsledku anglicky

Genetic studies of type 1 diabetes (T1D) have identified 50 susceptibility regions(1,2), finding major pathways contributing to risk(3), with some loci shared across immune disorders(4-6). To make genetic comparisons across autoimmune disorders as informative as possible, a dense genotyping array, the Immunochip, was developed, from which we identified four new T1D-associated regions (P < 5 x 10(-8)). A comparative analysis with 15 immune diseases showed that T1D is more similar genetically to other autoantibody-positive diseases, significantly most similar to juvenile idiopathic arthritis and significantly least similar to ulcerative colitis, and provided support for three additional new T1D risk loci. Using a Bayesian approach, we defined credible sets for the T1D-associated SNPs. The associated SNPs localized to enhancer sequences active in thymus, T and B cells, and CD34(+) stem cells. Enhancer-promoter interactions can now be analyzed in these cell types to identify which particul

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

—

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2015

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Nature Genetics

ISSN

1061-4036

e-ISSN

—

Svazek periodika

47

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

381-"U199"

Kód UT WoS článku

000351922900014

EID výsledku v databázi Scopus

2-s2.0-84930408328