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      PATZ1 is a DNA damage-responsive transcription factor that inhibits p53 function

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      Author
      Keskin, N.
      Deniz, E.
      Eryilmaz J.
      Un, M.
      Batur, T.
      Ersahin, T.
      Atalay, R.C.
      Sakaguchi, S.
      Ellmeier W.
      Erman, B.
      Date
      2015
      Source Title
      Molecular and Cellular Biology
      Print ISSN
      0270-7306
      Publisher
      American Society for Microbiology
      Volume
      35
      Issue
      10
      Pages
      1741 - 1753
      Language
      English
      Type
      Article
      Item Usage Stats
      118
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      119
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      Abstract
      Insults to cellular health cause p53 protein accumulation, and loss of p53 function leads to tumorigenesis. Thus, p53 has to be tightly controlled. Here we report that the BTB/POZ domain transcription factor PATZ1 (MAZR), previously known for its transcriptional suppressor functions in T lymphocytes, is a crucial regulator of p53. The novel role of PATZ1 as an inhibitor of the p53 protein marks its gene as a proto-oncogene. PATZ1-deficient cells have reduced proliferative capacity, which we assessed by transcriptome sequencing (RNA-Seq) and real-time cell growth rate analysis. PATZ1 modifies the expression of p53 target genes associated with cell proliferation gene ontology terms. Moreover, PATZ1 regulates several genes involved in cellular adhesion and morphogenesis. Significantly, treatment with the DNA damage-inducing drug doxorubicin results in the loss of the PATZ1 transcription factor as p53 accumulates. We find that PATZ1 binds to p53 and inhibits p53-dependent transcription activation. We examine the mechanism of this functional inhibitory interaction and demonstrate that PATZ1 excludes p53 from DNA binding. This study documents PATZ1 as a novel player in the p53 pathway. © 2015, American Society for Microbiology.
      Keywords
      doxorubicin
      heterodimer
      protein p53
      transcription factor
      transcription factor patz1
      unclassified drug
      animal cell
      Article
      carboxy terminal sequence
      cell adhesion
      cell growth
      DNA damage
      down regulation
      embryo
      gene ontology
      human
      human cell
      morphogenesis
      mouse
      nonhuman
      priority journal
      protein binding
      protein domain
      protein expression
      protein function
      protein interaction
      RNA sequence
      transcription initiation
      Permalink
      http://hdl.handle.net/11693/22703
      Published Version (Please cite this version)
      http://dx.doi.org/10.1128/MCB.01475-14
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      • Department of Molecular Biology and Genetics 442
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