On the development of biophysical models for space radiation risk assessment.
Experimental techniques in molecular biology are being applied to study biological risks from space radiation. The use of molecular assays presents a challenge to biophysical models which in the past have relied on descriptions of energy deposition and phenomenological treatments of repair. We describe a biochemical kinetics model of cell cycle control and DNA damage response proteins in order to model cellular responses to radiation exposures. Using models of cyclin-cdk, pRB, E2F's, p53, and G1 inhibitors we show that simulations of cell cycle populations and G1 arrest can be described by our biochemical approach. We consider radiation damaged DNA as a substrate for signal transduction processes and consider a dose and dose-rate reduction effectiveness factor (DDREF) for protein expression.
Cucinotta
F A
FA
NASA, Johnson Space Center, Houston, TX 77058-0001, USA.
Dicello
J F
JF
D002453:Cell Cycle / Q000502:physiology / Q000528:radiation effects; D003359:Cosmic Radiation; D016213:Cyclins / Q000096:biosynthesis / Q000502:physiology*; D004249:DNA Damage; D004260:DNA Repair; D016193:G1 Phase / Q000502:physiology / Q000528:radiation effects; D005786:Gene Expression Regulation / Q000528:radiation effects; D016158:Genes, p53; D008954:Models, Biological; D008958:Models, Molecular; D008967:Molecular Biology / Q000379:methods; D018570:Risk Assessment; D015398:Signal Transduction; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D016213:Cyclins; D016159:Tumor Suppressor Protein p53