title: Cell cycle regulators guide mitochondrial activity in radiation-induced adaptive response.
abstract: CONCLUSIONS
  There are accruing concerns on potential genotoxic agents present in the environment including low-dose ionizing radiation (LDIR) that naturally exists on earth's surface and atmosphere and is frequently used in medical diagnosis and nuclear industry. Although its long-term health risk is being evaluated and remains controversial, LDIR is shown to induce temporary but significant adaptive responses in mammalian cells and animals. The mechanisms guiding the mitochondrial function in LDIR-induced adaptive response represent a unique communication between DNA damage and cellular metabolism. Elucidation of the LDIR-regulated mitochondrial activity may reveal new mechanisms adjusting cellular function to cope with hazardous environmental stress.
  
  
  BACKGROUND
  Key cell cycle regulators, including Cyclin D1/CDK4 and Cyclin B1/cyclin-dependent kinase 1 (CDK1) complexes, are actively involved in the regulation of mitochondrial functions via phosphorylation of their mitochondrial targets. Accumulating new evidence supports a concept that the Cyclin B1/CDK1 complex acts as a mediator in the cross talk between radiation-induced DNA damage and mitochondrial functions to coordinate cellular responses to low-level genotoxic stresses.
  
  
  RESULTS
  The LDIR-mediated mitochondrial activity via Cyclin B1/CDK1 regulation is an irreplaceable network that is able to harmonize vital cellular functions with adjusted mitochondrial metabolism to enhance cellular homeostasis.
  
  
  CONCLUSIONS
  Further investigation of the coordinative mechanism that regulates mitochondrial activities in sublethal stress conditions, including LDIR, will reveal new insights of how cells cope with genotoxic injury and will be vital for future targeted therapeutic interventions that reduce environmental injury and cancer risk.
authors.affiliation: Department of Radiation Oncology, NCI-Designated Comprehensive Cancer Center, University of California at Davis , Sacramento, California.
authors.forename: Aris T
authors.initials: AT
authors.lastname: Alexandrou
authors.forename: Jian Jian
authors.initials: JJ
authors.lastname: Li
mesh_terms: D000220:Adaptation, Biological / Q000528:radiation effects*; D000818:Animals; D017209:Apoptosis / Q000502:physiology / Q000528:radiation effects; D002453:Cell Cycle / Q000502:physiology / Q000528:radiation effects; D018797:Cell Cycle Proteins / Q000235:genetics* / Q000378:metabolism*; D018844:Cyclin-Dependent Kinases / Q000378:metabolism; D016213:Cyclins / Q000378:metabolism; D006801:Humans; D008928:Mitochondria / Q000502:physiology* / Q000528:radiation effects*; D063154:Mitochondrial Dynamics / Q000502:physiology / Q000528:radiation effects; D018832:Molecular Chaperones / Q000378:metabolism; D010084:Oxidation-Reduction; D010085:Oxidative Phosphorylation / Q000528:radiation effects; D021381:Protein Transport; D011829:Radiation Dosage; D011839:Radiation, Ionizing; D015398:Signal Transduction / Q000528:radiation effects
chemical_list: D018797:Cell Cycle Proteins; D016213:Cyclins; D018832:Molecular Chaperones; D018844:Cyclin-Dependent Kinases