rdf-syntax-grammar
mods:
  schema location: http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
  title info:
    title: Mechanisms of transcriptional activation of estrogen responsive genes in breast cancer cells
  name:
    name part: Chen, Chien-Cheng.
    role:
      role term: creator
  name:
    name part: Safe, Stephen H.
    role:
      role term: thesis advisor.
  type of resource: text
  genre: bibliography
  origin info:
    place:
      place term: txu
    date issued: 2010
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: electronic
    form: remote
    extent: 1 online resource.
  abstract: Estrogen receptor (ER) acts as a ligand-activated transcription factor that regulates the expression of genes. The genomic mechanisms of ER action include ligand-induced dimerization of ER which binds estrogen responsive elements (EREs) in the promoters of target genes. There are also nongenomic mechanisms of ER action which are associated with membrane bound or cytosol ER-dependent activation of various protein-kinase cascades which also influence expression of target genes. Egr-1 is an immediate-early gene induced by 17B-estradiol (E2) in the rodent uterus and breast cancer cells. Deletion analysis of the Egr-1 promoter identified a minimal E2-responsive region that contained serum response element (SRE3) which bound Elk-1 and serum response factor (SRF) in gel mobility shift assays. Hormone-responsiveness of Egr-1 in MCF-7 cells was specifically inhibited by PD98059, a MAPKK inhibitor, but not by LY294002, an inhibitor of PI3-K. These results contrasted with the hormone-dependent activation of the SRE in the c-fos promoter, which was inhibited by both PD98059 and LY294002, suggesting that Egr-1, like c-fos, is activated through non-genomic pathways of estrogen action but through activation of different kinases. COUP-TFs are orphan nuclear receptors expressed in a variety of tissues where they regulate biological functions and organogenesis. In this study, we investigated coactivation of ERa by COUP-TF1 in cell lines transiently cotransfected with the pERE3 construct. COUP-TFI coactivated ERał-mediated transactivation, but unlike many other coactivators, COUP-TFI also enhanced transactivation of ERa when cells were cotransfected with the TAF1-ERa mutant or the 19c-ERa mutant. These data indicate that helix 12 of ERa is not required for coactivation by COUP-TFI when AF-1 of ERa is intact. However, when the AF-1 of ERa is deleted, the intact AF-2 function is required for coactivation by COUP-TFI. Analysis of multiple COUP-TFI deletion mutants showed that the DNA-bin…
  note: by Chien-Cheng Chen.
  note: "Major Subject: Toxicology"
  note: Title from author supplied metadata (automated record created 2010-03-12 12:08:51).
  note: Electronic resource.
  note: Doctor of Philosophy Texas A&M University 2006 http://hdl.handle.net/1969.1/ETD-TAMU-1869
  note: Includes bibliographical references.
  note: Text (Dissertation)
  subject:
    topic: Major toxicology
  subject:
    topic: Transcription
  subject:
    topic: Estrogen
  identifier: http://hdl.handle.net/1969.1/ETD-TAMU-1869
  record info:
    record content source: TXA
    record creation date: 100428
    record change date: 20151201150143.0
    record identifier: in00002575427