Computational model of the modulation of gene expression following DNA damage.
High linear energy transfer (LET) radiation, such as heavy ions or neutrons, has an increased biological effectiveness compared to X rays for gene mutation, genomic instability, and carcinogenesis. In the traditional paradigm, mutations or chromosomal aberrations are causative of late effects. However, in recent years experimental evidence has demonstrated the important role of the description of the modification of gene expression by radiation in understanding the mechanisms of radiation action. In this report, approaches are discussed to the mathematical description of mRNA and protein expression kinetics following DNA damage. Several hypotheses for models of radiation modulation of protein expression are discussed including possible non-linear processes that evolve from the linear dose responses that follow the initial DNA damage produced by radiation.
Cucinotta
F A
FA
NASA Johnson Space Center, Houston, TX, USA. Francis.A.Cucinotta1@jsc.nasa.gorv
Dicello
J F
JF
Nikjoo
H
H
Cherubini
R
R
D002455:Cell Division / Q000528:radiation effects; D004247:DNA / Q000235:genetics / Q000528:radiation effects; D004249:DNA Damage / Q000528:radiation effects*; D005786:Gene Expression Regulation / Q000528:radiation effects*; D047908:Intracellular Signaling Peptides and Proteins; D007700:Kinetics; D008954:Models, Biological; D011506:Proteins / Q000235:genetics / Q000528:radiation effects; D011853:Radiobiology / Q000379:methods; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000528:radiation effects; D000097642:GADD45 Proteins
D004247:DNA; D047908:Intracellular Signaling Peptides and Proteins; D011506:Proteins; D016159:Tumor Suppressor Protein p53; D000097642:GADD45 Proteins
NASA Center JSC; NASA Discipline Radiation Health; Non-NASA Center