DESCRIPTION:

List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Psoriasis. The EFO term psoriasis was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.

LABEL:

GWAS: psoriasis

SCORE TYPE:

P-Value

DATE ADDED:

2017-05-02

DATE UPDATED:

2020-05-06

SPECIES:

AUTHORS:

RP Nair, KC Duffin, C Helms, J Ding, PE Stuart, D Goldgar, JE Gudjonsson, Y Li, T Tejasvi, BJ Feng, A Ruether, S Schreiber, M Weichenthal, D Gladman, P Rahman, SJ Schrodi, S Prahalad, SL Guthery, J Fischer, W Liao, PY Kwok, A Menter, GM Lathrop, CA Wise, AB Begovich, JJ Voorhees, JT Elder, GG Krueger, AM Bowcock, GR Abecasis

TITLE:

Genome-wide scan reveals association of psoriasis with IL-23 and NF-kappaB pathways.

JOURNAL:

Nature genetics Feb 2009, Vol 41, pp. 199-204

ABSTRACT:

Psoriasis is a common immune-mediated disorder that affects the skin, nails and joints. To identify psoriasis susceptibility loci, we genotyped 438,670 SNPs in 1,409 psoriasis cases and 1,436 controls of European ancestry. We followed up 21 promising SNPs in 5,048 psoriasis cases and 5,041 controls. Our results provide strong support for the association of at least seven genetic loci and psoriasis (each with combined P < 5 x 10(-8)). Loci with confirmed association include HLA-C, three genes involved in IL-23 signaling (IL23A, IL23R, IL12B), two genes that act downstream of TNF-alpha and regulate NF-kappaB signaling (TNIP1, TNFAIP3) and two genes involved in the modulation of Th2 immune responses (IL4, IL13). Although the proteins encoded in these loci are known to interact biologically, we found no evidence for epistasis between associated SNPs. Our results expand the catalog of genetic loci implicated in psoriasis susceptibility and suggest priority targets for study in other auto-immune disorders. PUBMED: 19169254
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