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Regulation of retinoblastoma protein functions by ectopic expression of human cyclins

Academic Article
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Overview

authors

  • Hinds, P. W.
  • Mittnacht, S.
  • Dulic, V.
  • Arnold, A.
  • Reed, Steven
  • Weinberg, R. A.

publication date

  • September 1992

journal

  • Cell  Journal

abstract

  • The retinoblastoma susceptibility gene (RB) product, the retinoblastoma protein (pRb), functions as a regulator of cell proliferation. Introduction of the RB gene into SAOS-2 osteosarcoma cells, which lack functional pRb, prevents cell cycle progression. Such growth-suppressive functions can be modulated by phosphorylation of pRb, which occurs via cell cycle-regulated kinases. We show that constitutively expressed cyclins A and E can overcome pRb-mediated suppression of proliferation. pRb becomes hyperphosphorylated in cells overexpressing these cyclins, and this phosphorylation is essential for cyclin A- and cyclin E-mediated rescue of pRb-blocked cells. This suggests that G1 and S phase cyclins can act as regulators of pRb function in the cell cycle by promoting pRb phosphorylation.

subject areas

  • Cell Nucleus
  • Cyclins
  • G1 Phase
  • Gene Expression
  • Genetic Vectors
  • Humans
  • Mutation
  • Phenotype
  • Phosphorylation
  • Protein Kinases
  • Recombinant Proteins
  • Retinoblastoma Protein
  • Transfection
  • Tumor Cells, Cultured
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Identity

International Standard Serial Number (ISSN)

  • 0092-8674

Digital Object Identifier (DOI)

  • 10.1016/0092-8674(92)90249-c

PubMed ID

  • 1388095
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Additional Document Info

start page

  • 993

end page

  • 1006

volume

  • 70

issue

  • 6

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