title: The -431C>T polymorphism of thymus and activation-regulated chemokine increases the promoter activity but is not associated with susceptibility to atopic dermatitis in Japanese patients.
abstract: BACKGROUND
  Thymus and activation-regulated chemokine (TARC) plays an important role in the pathogenesis of atopic dermatitis (AD). We recently detected the single nucleotide polymorphism (SNP) (-431C>T) in the 5'-flanking region of TARC gene.
  
  
  OBJECTIVE
  To examine whether the -431C>T SNP of the TARC gene is associated with susceptibility to AD and whether it affects the promoter activity of the TARC gene.
  
  
  METHODS
  We investigated the genotype and allele frequencies of the SNP in 193 AD patients and 158 healthy controls by polymerase chain reaction-restriction fragment length polymorphism method. We compared the promoter activities between TARC promoter carrying 431C and that carrying -431T by transient-transfection assay in DJM-1 cell line.
  
  
  RESULTS
  There were no significant differences in genotype or allele frequencies between AD patients and controls (genotype: P = 0.38, allele: P = 0.22). Luciferase activity was higher in -431T constructs than in -431C constructs (2.3-fold, P = 9.5 x 10(-6)).
  
  
  CONCLUSIONS
  These results suggest that the -431C>T SNP of the TARC gene enhances the promoter activity of TARC gene but is not associated with susceptibility to AD in Japanese population.
authors.affiliation: Department of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan. ytsun-tky@umin.ac.jp
authors.forename: Yuichiro
authors.initials: Y
authors.lastname: Tsunemi
authors.forename: Mayumi
authors.initials: M
authors.lastname: Komine
authors.forename: Takashi
authors.initials: T
authors.lastname: Sekiya
authors.forename: Hidehisa
authors.initials: H
authors.lastname: Saeki
authors.forename: Koichiro
authors.initials: K
authors.lastname: Nakamura
authors.forename: Koichi
authors.initials: K
authors.lastname: Hirai
authors.forename: Takashi
authors.initials: T
authors.lastname: Kakinuma
authors.forename: Shinji
authors.initials: S
authors.lastname: Kagami
authors.forename: Hideki
authors.initials: H
authors.lastname: Fujita
authors.forename: Noriko
authors.initials: N
authors.lastname: Asano
authors.forename: Yuka
authors.initials: Y
authors.lastname: Tanida
authors.forename: Motoshi
authors.initials: M
authors.lastname: Wakugawa
authors.forename: Hideshi
authors.initials: H
authors.lastname: Torii
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Tamaki
mesh_terms: D000293:Adolescent; D000328:Adult; D000483:Alleles; D054414:Chemokine CCL17; D019742:Chemokines, CC / Q000235:genetics* / Q000502:physiology*; D002648:Child; D003876:Dermatitis, Atopic / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D007564:Japan; D008156:Luciferases / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D020641:Polymorphism, Single Nucleotide; D011401:Promoter Regions, Genetic; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014162:Transfection
chemical_list: C106230:CCL17 protein, human; D054414:Chemokine CCL17; D019742:Chemokines, CC; D012333:RNA, Messenger; D008156:Luciferases