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Over four decades of the studies of molecular mechanisms, and enzymes, assuring genetic stability (DNA repair) and variability (mutagenesis and recombination) were crowned by direct visualization of emerging individual mutation and recombination events in single living bacterial cells, in real time. The interest in extreme radiation resistance of the bacterium Deinococcus radiodurans changed the course of Radman's research. His group discovered the mechanism of repair of over one thousand of DNA double-strand breaks per D. radiodurns cell and found that the evolved protection of proteins against oxidative damage accounts for extreme biological robustness. Radman's group showed that biological function can be reduced or destroyed directly by oxidative protein damage (and not only indirectly by mutation). Hence, the view of cell function, aging and survival changed from DNA-centric to protein-centric. Having found that most proteins from aerobic organisms are quasi inoxidable, Miroslav Radman's laboratory studies the causes of protein damage and explores how silent mutations (polymorphisms) sensitize the affected proteins to oxidation and therefore predispose to relevant age-related disease. Furthermore, Radman studies now the mechanism of expression of aging and disease phenotypes and why is long latency of age-related diseases shortened by chronic inflammation. The long term goal of this research is the mitigation of all age-related diseases by prevention and healing by phenotypic reversion. This approach aims to reduce disease initiation (at the genome level) and extend its latency period (at proteome level) to delay the onset of disease, or revert the disease back to health.
研究兴趣
论文共 245 篇作者统计合作学者相似作者
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Advances in Redox Research (2024)
European journal of dermatology EJDno. 4 (2024): 355-360
Free radical biology & medicine (2023): 106-110
Research Square (Research Square) (2023)
Frontiers in genetics (2022)
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作者统计
#Papers: 244
#Citation: 19938
H-Index: 68
G-Index: 138
Sociability: 6
Diversity: 3
Activity: 18
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