Macrophage migration inhibitory factor coordinates DNA damage response with the proteasomal control of the cell cycle

Cell Cycle. 2007 May 2;6(9):1030-4. doi: 10.4161/cc.6.9.4163. Epub 2007 May 20.

Abstract

Proper repair of DNA damage is critical for protecting genomic stability, cellular viability and suppression of tumorigenesis. Both p53-dependent and p53-independent pathways have evolved to coordinate the cellular response following DNA damage. In this review, we highlight the importance of the ubiquitously expressed protein macrophage migration inhibitory factor (MIF) for an appropriate response to DNA damage. We discuss the mechanisms by which MIF affects the activity of the ubiquitin-proteasome system, and how this impacts on the integrity of the genome and on cancer.

Publication types

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

MeSH terms

  • Animals
  • Cell Cycle* / genetics
  • Cell Cycle* / physiology
  • DNA Damage / physiology*
  • G2 Phase
  • Genes, cdc
  • Humans
  • In Situ Hybridization, Fluorescence
  • Macrophage Migration-Inhibitory Factors / genetics
  • Macrophage Migration-Inhibitory Factors / physiology*
  • Models, Biological
  • Neoplasms / genetics
  • Neoplasms / metabolism
  • Proteasome Endopeptidase Complex / metabolism*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • Ubiquitin / metabolism

Substances

  • Macrophage Migration-Inhibitory Factors
  • Tumor Suppressor Protein p53
  • Ubiquitin
  • Proteasome Endopeptidase Complex