Restarting the cell cycle when the checkpoint comes to a halt.
The DNA damage checkpoint coordinates a block in cell proliferation with the DNA repair process that follows when lesions are inflicted on the genome. However, we do not know exactly how cell division can recommence following a DNA damage-induced arrest. Recent work from our lab has identified Polo-like kinase-1 and Cdc25B as two essential components of the machinery that sets the cell division process back in motion when the checkpoint response is abrogated. Here, we discuss these novel insights and discuss their possible implications for the treatment of cancer.
van Vugt
Marcel A T M
MA
Department of Medical Oncology, University Medical Center Utrecht, Utrecht, the Netherlands.
Bràs
Alexandra
A
Medema
René H
RH
D000818:Animals; D002453:Cell Cycle / Q000502:physiology; D018797:Cell Cycle Proteins / Q000502:physiology; D004249:DNA Damage / Q000502:physiology*; D018816:Genes, cdc / Q000502:physiology*; D006801:Humans; D009369:Neoplasms / Q000235:genetics* / Q000473:pathology; D011494:Protein Kinases / Q000502:physiology; D017346:Protein Serine-Threonine Kinases; D011518:Proto-Oncogene Proteins / Q000502:physiology; D020687:cdc25 Phosphatases / Q000502:physiology; D000097869:Polo-Like Kinase 1
D018797:Cell Cycle Proteins; D011494:Protein Kinases; D017346:Protein Serine-Threonine Kinases; D011518:Proto-Oncogene Proteins; D020687:cdc25 Phosphatases; D000097869:Polo-Like Kinase 1; C517008:CDC25B protein, human