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Sökning: WFRF:(Namjou Khales B) > (2022) > Genetic regulation ...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003950naa a2200865 4500
001oai:prod.swepub.kib.ki.se:151257225
003SwePub
008240701s2022 | |||||||||||000 ||eng|
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1512572252 URI
024a https://doi.org/10.1038/s41467-022-34456-62 DOI
040 a (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Liu, LL4 aut
2451 0a Genetic regulation of serum IgA levels and susceptibility to common immune, infectious, kidney, and cardio-metabolic traits
264 c 2022-11-11
264 1b 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.
700a Khan, A4 aut
700a Sanchez-Rodriguez, E4 aut
700a Zanoni, F4 aut
700a Li, YF4 aut
700a Steers, N4 aut
700a Balderes, O4 aut
700a Zhang, JY4 aut
700a Krithivasan, P4 aut
700a LeDesma, RA4 aut
700a Fischman, C4 aut
700a Hebbring, SJ4 aut
700a Harley, JB4 aut
700a Moncrieffe, H4 aut
700a Kottyan, LC4 aut
700a Namjou-Khales, B4 aut
700a Walunas, TL4 aut
700a Knevel, R4 aut
700a Raychaudhuri, S4 aut
700a Karlson, EW4 aut
700a Denny, JC4 aut
700a Stanaway, IB4 aut
700a Crosslin, D4 aut
700a Rauen, T4 aut
700a Floege, J4 aut
700a Eitner, F4 aut
700a Moldoveanu, Z4 aut
700a Reily, C4 aut
700a Knoppova, B4 aut
700a Hall, S4 aut
700a Sheff, JT4 aut
700a Julian, BA4 aut
700a Wyatt, RJ4 aut
700a Suzuki, H4 aut
700a Xie, JY4 aut
700a Chen, N4 aut
700a Zhou, XJ4 aut
700a Zhang, H4 aut
700a Hammarstrom, Lu Karolinska Institutet4 aut
700a Viktorin, A4 aut
700a Magnusson, PKEu Karolinska Institutet4 aut
700a Shang, N4 aut
700a Hripcsak, G4 aut
700a Weng, CH4 aut
700a Rundek, T4 aut
700a Elkind, MSV4 aut
700a Oelsner, EC4 aut
700a Barr, RG4 aut
700a Ionita-Laza, I4 aut
700a Novak, J4 aut
700a Gharavi, AG4 aut
700a Kiryluk, K4 aut
710a Karolinska Institutet4 org
773t Nature communicationsd : Springer Science and Business Media LLCg 13:1, s. 6859-q 13:1<6859-x 2041-1723
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:151257225
8564 8u https://doi.org/10.1038/s41467-022-34456-6

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