title: Nkx3.1 controls the DNA repair response in the mouse prostate.
abstract: BACKGROUND
  The human prostate tumor suppressor NKX3.1 mediates the DNA repair response and interacts with the androgen receptor to assure faithful completion of transcription thereby protecting against TMPRSS2-ERG gene fusion. To determine directly the effect of Nkx3.1 in vivo we studied the DNA repair response in prostates of mice with targeted deletion of Nkx3.1.
  
  
  METHODS
  Using both drug-induced DNA damage and γ-irradiation, we assayed expression of γ-histone 2AX at time points up to 24 hr after induction of DNA damage.
  
  
  RESULTS
  We demonstrated that expression of Nkx3.1 influenced both the timing and magnitude of the DNA damage response in the prostate.
  
  
  CONCLUSIONS
  Nkx3.1 affects the DNA damage response in the murine prostate and is haploinsufficient for this phenotype.
authors.affiliation: Department of Medicine and Pathology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York.
authors.forename: Hailan
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Medicine and Pathology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York.|Department of Statistics, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York.
authors.forename: Tian
authors.initials: T
authors.lastname: Zheng
authors.affiliation: Department of Medicine and Pathology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York.|Department of Developmental and Cell Biology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York.
authors.forename: Chee Wai
authors.initials: CW
authors.lastname: Chua
authors.affiliation: Department of Medicine and Pathology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York.|Department of Developmental and Cell Biology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York.
authors.forename: Michael
authors.initials: M
authors.lastname: Shen
authors.affiliation: Department of Medicine and Pathology, Columbia University Medical Center, Herbert Irving Comprehensive Cancer Center, Columbia University, New York City, New York.
authors.forename: Edward P
authors.initials: EP
authors.lastname: Gelmann
mesh_terms: D000818:Animals; D004247:DNA / Q000187:drug effects / Q000528:radiation effects; D004249:DNA Damage; D004260:DNA Repair / Q000502:physiology*; D005047:Etoposide / Q000494:pharmacology; D005720:Gamma Rays; D018398:Homeodomain Proteins / Q000235:genetics / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008817:Mice, Mutant Strains; D016685:Mitomycin / Q000494:pharmacology; D011467:Prostate / Q000378:metabolism*; D014157:Transcription Factors / Q000172:deficiency / Q000235:genetics / Q000502:physiology*
chemical_list: D018398:Homeodomain Proteins; C102837:Nkx3-1 protein, mouse; D014157:Transcription Factors; D016685:Mitomycin; D005047:Etoposide; D004247:DNA
keywords: DNA repair; NKX3.1; haploinsufficiency; γhistone 2AX