title: On the development of biophysical models for space radiation risk assessment.
abstract: 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.
authors.affiliation: NASA, Johnson Space Center, Houston, TX 77058-0001, USA.
authors.forename: F A
authors.initials: FA
authors.lastname: Cucinotta
authors.forename: J F
authors.initials: JF
authors.lastname: Dicello
mesh_terms: 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
chemical_list: D016213:Cyclins; D016159:Tumor Suppressor Protein p53