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P53-dependent inhibition of cyclin-dependent kinase-activities in human fibroblasts during radiation-induced g1 arrest

Academic Article
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Overview

authors

  • Dulic, V.
  • Kaufmann, W. K.
  • Wilson, S. J.
  • Tlsty, T. D.
  • Lees, E.
  • Harper, J. W.
  • Elledge, S. J.
  • Reed, Steven

publication date

  • March 1994

journal

  • Cell  Journal

abstract

  • gamma-Irradiation of human diploid fibroblasts in the G1 interval caused arrest of the cell cycle prior to S phase. This cell cycle block was correlated with a lack of activation of both cyclin E-Cyclin-dependent kinase 2 (Cdk2) and cyclin A-Cdk2 kinases and depended on wild-type p53. Although the accumulation of cyclin A was strongly inhibited in gamma-irradiated cells, cyclin E accumulated and bound Cdk2 at normal levels but remained in an inactive state. We found that both whole-cell lysates and inactive cyclin E-Cdk2 complexes prepared from irradiated cells contained an activity capable of inactivating cyclin E-Cdk2 complexes. The protein responsible for this activity was shown to be p21CIP1/WAF1, recently described as a p53-inducible Cdk inhibitor. Our data suggest a model in which ionizing radiation confers G1 arrest via the p53-mediated induction of a Cdk inhibitor protein.

subject areas

  • Base Sequence
  • Cells, Cultured
  • Cyclin D1
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • Enzyme Activation
  • Fibroblasts
  • G1 Phase
  • Gamma Rays
  • Humans
  • Male
  • Molecular Sequence Data
  • Oncogene Proteins
  • Protein Kinase Inhibitors
  • Protein Kinases
  • Retinoblastoma Protein
  • Tumor Suppressor Protein p53
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Identity

International Standard Serial Number (ISSN)

  • 0092-8674

Digital Object Identifier (DOI)

  • 10.1016/0092-8674(94)90379-4

PubMed ID

  • 8137420
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Additional Document Info

start page

  • 1013

end page

  • 1023

volume

  • 76

issue

  • 6

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