Sökning: onr:"swepub:oai:prod.swepub.kib.ki.se:151257225" > Genetic regulation ...
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000 | 03950naa a2200865 4500 | |
001 | oai:prod.swepub.kib.ki.se:151257225 | |
003 | SwePub | |
008 | 240913s2022 | |||||||||||000 ||eng| | |
024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:1512572252 URI |
024 | 7 | a https://doi.org/10.1038/s41467-022-34456-62 DOI |
040 | a (SwePub)ki | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Liu, LL4 aut |
245 | 1 0 | a Genetic regulation of serum IgA levels and susceptibility to common immune, infectious, kidney, and cardio-metabolic traits |
264 | c 2022-11-11 | |
264 | 1 | b Springer Science and Business Media LLC,c 2022 |
520 | a Immunoglobulin A (IgA) mediates mucosal responses to food antigens and the intestinal microbiome and is involved in susceptibility to mucosal pathogens, celiac disease, inflammatory bowel disease, and IgA nephropathy. We performed a genome-wide association study of serum IgA levels in 41,263 individuals of diverse ancestries and identified 20 genome-wide significant loci, including 9 known and 11 novel loci. Co-localization analyses with expression QTLs prioritized candidate genes for 14 of 20 significant loci. Most loci encoded genes that produced immune defects and IgA abnormalities when genetically manipulated in mice. We also observed positive genetic correlations of serum IgA levels with IgA nephropathy, type 2 diabetes, and body mass index, and negative correlations with celiac disease, inflammatory bowel disease, and several infections. Mendelian randomization supported elevated serum IgA as a causal factor in IgA nephropathy. African ancestry was consistently associated with higher serum IgA levels and greater frequency of IgA-increasing alleles compared to other ancestries. Our findings provide novel insights into the genetic regulation of IgA levels and its potential role in human disease. | |
700 | 1 | a Khan, A4 aut |
700 | 1 | a Sanchez-Rodriguez, E4 aut |
700 | 1 | a Zanoni, F4 aut |
700 | 1 | a Li, YF4 aut |
700 | 1 | a Steers, N4 aut |
700 | 1 | a Balderes, O4 aut |
700 | 1 | a Zhang, JY4 aut |
700 | 1 | a Krithivasan, P4 aut |
700 | 1 | a LeDesma, RA4 aut |
700 | 1 | a Fischman, C4 aut |
700 | 1 | a Hebbring, SJ4 aut |
700 | 1 | a Harley, JB4 aut |
700 | 1 | a Moncrieffe, H4 aut |
700 | 1 | a Kottyan, LC4 aut |
700 | 1 | a Namjou-Khales, B4 aut |
700 | 1 | a Walunas, TL4 aut |
700 | 1 | a Knevel, R4 aut |
700 | 1 | a Raychaudhuri, S4 aut |
700 | 1 | a Karlson, EW4 aut |
700 | 1 | a Denny, JC4 aut |
700 | 1 | a Stanaway, IB4 aut |
700 | 1 | a Crosslin, D4 aut |
700 | 1 | a Rauen, T4 aut |
700 | 1 | a Floege, J4 aut |
700 | 1 | a Eitner, F4 aut |
700 | 1 | a Moldoveanu, Z4 aut |
700 | 1 | a Reily, C4 aut |
700 | 1 | a Knoppova, B4 aut |
700 | 1 | a Hall, S4 aut |
700 | 1 | a Sheff, JT4 aut |
700 | 1 | a Julian, BA4 aut |
700 | 1 | a Wyatt, RJ4 aut |
700 | 1 | a Suzuki, H4 aut |
700 | 1 | a Xie, JY4 aut |
700 | 1 | a Chen, N4 aut |
700 | 1 | a Zhou, XJ4 aut |
700 | 1 | a Zhang, H4 aut |
700 | 1 | a Hammarstrom, Lu Karolinska Institutet4 aut |
700 | 1 | a Viktorin, A4 aut |
700 | 1 | a Magnusson, PKEu Karolinska Institutet4 aut |
700 | 1 | a Shang, N4 aut |
700 | 1 | a Hripcsak, G4 aut |
700 | 1 | a Weng, CH4 aut |
700 | 1 | a Rundek, T4 aut |
700 | 1 | a Elkind, MSV4 aut |
700 | 1 | a Oelsner, EC4 aut |
700 | 1 | a Barr, RG4 aut |
700 | 1 | a Ionita-Laza, I4 aut |
700 | 1 | a Novak, J4 aut |
700 | 1 | a Gharavi, AG4 aut |
700 | 1 | a Kiryluk, K4 aut |
710 | 2 | a Karolinska Institutet4 org |
773 | 0 | t Nature communicationsd : Springer Science and Business Media LLCg 13:1, s. 6859-q 13:1<6859-x 2041-1723 |
856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:151257225 |
856 | 4 8 | u https://doi.org/10.1038/s41467-022-34456-6 |
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