Psoriasis 2 ist eine autosomal dominante systemische autoinflammatorische Erkrankung mir vorwiegend kutaner Manifestation, die durch Mutationen im CARD14-Gen hervorgerufen wird.
Helms C et. al. (2003) A putative RUNX1 binding site variant between SLC9A3R1 and NAT9 is associated with susceptibility to psoriasis.
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.
Tomfohrde J et. al. (1994) Gene for familial psoriasis susceptibility mapped to the distal end of human chromosome 17q.
Hwu WL et. al. (2005) Mapping of psoriasis to 17q terminus.
Jordan CT et. al. (2012) PSORS2 is due to mutations in CARD14.
Jordan CT et al. (2012) Rare and common variants in CARD14, encoding an epidermal regulator of NF-kappaB, in psoriasis.
Nair RP et. al. () Scanning chromosome 17 for psoriasis susceptibility: lack of evidence for a distal 17q locus.
Matthews D et. al. (1995) Confirmation of genetic heterogeneity in familial psoriasis.
Enlund F et al. (1999) Analysis of three suggested psoriasis susceptibility loci in a large Swedish set of families: confirmation of linkage to chromosome 6p (HLA region), and to 17q, but not to 4q.
Speckman RA et. al. (2003) Novel immunoglobulin superfamily gene cluster, mapping to a region of human chromosome 17q25, linked to psoriasis susceptibility.
Capon F et. al. (2004) Genetic analysis of PSORS2 markers in a UK dataset supports the association between RAPTOR SNPs and familial psoriasis.
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.
Giardina E et. al. (2006) PSORS2 markers are not associated with psoriatic arthritis in the Italian population.