Deficiency of G1 regulators P53, P21Cip1 and/or pRb decreases hepatocyte sensitivity to TGFbeta cell cycle arrest

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Abstract

TGFbeta is critical to control hepatocyte proliferation by inducing G1-growth arrest through multiple pathways leading to inhibition of E2F transcription activity. The retinoblastoma protein pRb is a key controller of E2F activity and G1/S transition which can be inhibited in viral hepatitis. It is not known whether the impairment of pRb would alter the growth inhibitory potential of TGFbeta in disease. We asked how Rb-deficiency would affect responses to TGFbeta-induced cell cycle arrest.
Original languageEnglish
Pages (from-to)215
JournalBMC Cancer
Volume7
DOIs
Publication statusPublished - 2007

Keywords

  • Animals
  • Cell Cycle
  • Cell Proliferation
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cyclin-Dependent Kinase Inhibitor p21
  • E2F Transcription Factors
  • Fluorescent Antibody Technique
  • Hepatocytes
  • Male
  • Mice
  • Mice, Knockout
  • Proto-Oncogene Proteins c-myc
  • Retinoblastoma Protein
  • Signal Transduction
  • Transforming Growth Factor beta
  • Tumor Suppressor Protein p53

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