Ultraviolet B irradiation-induced G2 cell cycle arrest in human keratinocytes by inhibitory phosphorylation of the cdc2 cell cycle kinase

Oncogene. 1995 Nov 16;11(10):2151-6.


In response to genotoxic stress, cell cycle progression can be arrested at certain checkpoints which serve to maintain genomic integrity. We have investigated the mechanism of ultraviolet B (UVB) irradiation-induced cell cycle arrest in normal human keratinocytes and in the HaCaT keratinocyte cell line which carries mutant p53 tumour suppressor protein. While only normal keratinocytes showed a delay in G1 following sublethal UVB irradiation both cell types exhibited prolonged G2 arrest attributable to rapid inhibition of cyclin B-associated cdc2 kinase activity. This inhibition coincided with increased tyrosine phosphorylation of cdc2 and was reversed by the cdc25C phosphatase in vitro. The data indicate that UVB-induced G2 arrest in mammalian cells is mediated by inhibitory tyrosine phosphorylation of cdc2 and acts as a defense mechanism against DNA damage irrespective of the cells' p53 status.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • CDC2 Protein Kinase / antagonists & inhibitors
  • CDC2 Protein Kinase / metabolism
  • CDC2 Protein Kinase / radiation effects*
  • Cell Cycle / radiation effects
  • Cells, Cultured
  • Cyclins / metabolism
  • Dose-Response Relationship, Radiation
  • G2 Phase / radiation effects*
  • Humans
  • Keratinocytes / cytology
  • Keratinocytes / enzymology
  • Keratinocytes / radiation effects*
  • Mutation
  • Phosphorylation
  • Tumor Suppressor Protein p53 / genetics
  • Tyrosine / metabolism
  • Ultraviolet Rays / adverse effects*


  • Cyclins
  • Tumor Suppressor Protein p53
  • Tyrosine
  • CDC2 Protein Kinase