Psoriasis 2 is an autosomal dominant systemic autoinflamatory skin disease that is caused by mutations of the CARD14 gene.
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Helms C et. al. (2003) A putative RUNX1 binding site variant between SLC9A3R1 and NAT9 is associated with susceptibility to psoriasis. |
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Nair RP et al. (1997) Evidence for two psoriasis susceptibility loci (HLA and 17q) and two novel candidate regions (16q and 20p) by genome-wide scan. |
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Tomfohrde J et. al. (1994) Gene for familial psoriasis susceptibility mapped to the distal end of human chromosome 17q. |
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Hwu WL et. al. (2005) Mapping of psoriasis to 17q terminus. |
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Jordan CT et. al. (2012) PSORS2 is due to mutations in CARD14. |
6. |
Jordan CT et al. (2012) Rare and common variants in CARD14, encoding an epidermal regulator of NF-kappaB, in psoriasis. |
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Nair RP et. al. () Scanning chromosome 17 for psoriasis susceptibility: lack of evidence for a distal 17q locus. |
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Matthews D et. al. (1995) Confirmation of genetic heterogeneity in familial psoriasis. |
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Speckman RA et. al. (2003) Novel immunoglobulin superfamily gene cluster, mapping to a region of human chromosome 17q25, linked to psoriasis susceptibility. |
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Capon F et. al. (2004) Genetic analysis of PSORS2 markers in a UK dataset supports the association between RAPTOR SNPs and familial psoriasis. |
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Stuart P et. al. (2006) Analysis of RUNX1 binding site and RAPTOR polymorphisms in psoriasis: no evidence for association despite adequate power and evidence for linkage. |
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Giardina E et. al. (2006) PSORS2 markers are not associated with psoriatic arthritis in the Italian population. |