Inhibition of pRb phosphorylation and cell-cycle progression by a 20-residue peptide derived from p16CDKN2/INK4A

R Fåhraeus, J M Paramio, K L Ball, S Laín, D P Lane

Research output: Contribution to journalArticlepeer-review

Abstract

The CDKN2/INK4A tumour suppressor gene is deleted or mutated in a large number of human cancers. Overexpression of its product, p16, has been shown to block the transition through the G1/S phase of the cell cycle in a pRb-dependent fashion by inhibiting the cyclin D-dependent kinases cdk4 and cdk6. Reconstitution of p16 function in transformed cells is therefore an attractive target for anti-cancer drug design.
Original languageEnglish
Pages (from-to)84-91
Number of pages8
JournalCurrent biology : CB
Volume6
Issue number1
DOIs
Publication statusPublished - 1 Jan 1996

Keywords

  • Amino Acid Sequence
  • Carrier Proteins
  • Cell Cycle
  • Cyclin-Dependent Kinase 4
  • Cyclin-Dependent Kinase 6
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cyclin-Dependent Kinases
  • Molecular Sequence Data
  • Peptides
  • Phosphorylation
  • Protein-Serine-Threonine Kinases
  • Proto-Oncogene Proteins
  • Retinoblastoma Protein
  • S Phase

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