Systems-level approaches reveal conservation of trans-regulated genes in the rat and genetic determinants of blood pressure in humans
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F13%3A10210039" target="_blank" >RIV/00216208:11110/13:10210039 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/67985823:_____/13:00392100
Výsledek na webu
<a href="http://dx.doi.org/10.1093/cvr/cvs329" target="_blank" >http://dx.doi.org/10.1093/cvr/cvs329</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1093/cvr/cvs329" target="_blank" >10.1093/cvr/cvs329</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Systems-level approaches reveal conservation of trans-regulated genes in the rat and genetic determinants of blood pressure in humans
Popis výsledku v původním jazyce
Human genome-wide association studies (GWAS) of hypertension identified only few susceptibility loci with large effect that were replicated across populations. The vast majority of genes detected by GWAS has small effect and the regulatory mechanisms through which these genetic variants cause disease remain mostly unclear. Here, we used comparative genomics between human and an established rat model of hypertension to explore the transcriptional mechanisms mediating the effect of genes identified in 15hypertension GWAS. Time series analysis of radiotelemetric blood pressure (BP) was performed to assess 11 parameters of BP variation in recombinant inbred strains derived from the spontaneously hypertensive rat. BP data were integrated with approximate to 27 000 expression quantative trait loci (eQTLs) mapped across seven tissues, detecting 8000 significant associations between eQTL genes and BP variation in the rat. We then compiled a large catalogue of human genes from GWAS of hyperten
Název v anglickém jazyce
Systems-level approaches reveal conservation of trans-regulated genes in the rat and genetic determinants of blood pressure in humans
Popis výsledku anglicky
Human genome-wide association studies (GWAS) of hypertension identified only few susceptibility loci with large effect that were replicated across populations. The vast majority of genes detected by GWAS has small effect and the regulatory mechanisms through which these genetic variants cause disease remain mostly unclear. Here, we used comparative genomics between human and an established rat model of hypertension to explore the transcriptional mechanisms mediating the effect of genes identified in 15hypertension GWAS. Time series analysis of radiotelemetric blood pressure (BP) was performed to assess 11 parameters of BP variation in recombinant inbred strains derived from the spontaneously hypertensive rat. BP data were integrated with approximate to 27 000 expression quantative trait loci (eQTLs) mapped across seven tissues, detecting 8000 significant associations between eQTL genes and BP variation in the rat. We then compiled a large catalogue of human genes from GWAS of hyperten
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
FA - Kardiovaskulární nemoci včetně kardiochirurgie
OECD FORD obor
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Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
V - Vyzkumna aktivita podporovana z jinych verejnych zdroju
Ostatní
Rok uplatnění
2013
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Cardiovascular Research
ISSN
0008-6363
e-ISSN
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Svazek periodika
97
Číslo periodika v rámci svazku
4
Stát vydavatele periodika
NL - Nizozemsko
Počet stran výsledku
13
Strana od-do
653-665
Kód UT WoS článku
000315629700008
EID výsledku v databázi Scopus
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