Macrophage migration inhibitory factor coordinates DNA damage response with the proteasomal control of the cell cycle.
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.
Nemajerova
Alice
A
Department of Pathology, State University of New York at Stony Brook, Stony Brook, New York, USA.
Moll
Ute M
UM
Petrenko
Oleksi
O
Fingerle-Rowson
Günter
G
D000818:Animals; D002453:Cell Cycle / Q000235:genetics / Q000502:physiology; D004249:DNA Damage / Q000502:physiology*; D016195:G2 Phase; D018816:Genes, cdc; D006801:Humans; D017404:In Situ Hybridization, Fluorescence; D008263:Macrophage Migration-Inhibitory Factors / Q000235:genetics / Q000502:physiology*; D008954:Models, Biological; D009369:Neoplasms / Q000235:genetics / Q000378:metabolism; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D025801:Ubiquitin / Q000378:metabolism
D008263:Macrophage Migration-Inhibitory Factors; D016159:Tumor Suppressor Protein p53; D025801:Ubiquitin; D046988:Proteasome Endopeptidase Complex