Nagoya University · Medicine
Professor Masashi Tanaka's research lab focuses on molecular mechanisms underlying stress resistance and longevity, particularly in extremophile organisms like *Deinococcus radiodurans* and in mammalian models of aging and cardiovascular disease. The lab investigates DNA repair pathways, oxidative stress responses, and mitochondrial genetics, with a strong emphasis on identifying genes and molecular pathways that confer resilience to radiation, desiccation, and age-related pathologies. Key research directions include the role of stress-induced genes (e.g., ddrA, ddrB, pprA) in radiation resistance and the protective effects of enzymes like DDAH-I and SOD1 in mitigating inflammation and cardiac allograft dysfunction.
Figures are computed from collected data and may differ slightly.
During the first hour after a sublethal dose of ionizing radiation, 72 genes were upregulated threefold or higher in D. radiodurans R1. Thirty-three of these loci were also among a set of 73 genes expressed in R1 cultures recovering from desiccation. The five transcripts most highly induced in response to each stress are the same and encode proteins of unknown function. The genes (ddrA, ddrB, ddrC, ddrD, and pprA) corresponding to these transcripts were deleted, both alone and in all possible tw
We report results from the analysis of complete mitochondrial DNA (mtDNA) sequences from 112 Japanese semi-supercentenarians (aged above 105 years) combined with previously published data from 96 patients in each of three non-disease phenotypes: centenarians (99-105 years of age), healthy non-obese males, obese young males and four disease phenotypes, diabetics with and without angiopathy, and Alzheimer's and Parkinson's disease patients. We analyze the correlation between mitochondrial polymorp
Overexpression of DDAH-I attenuated oxidative stress, inflammatory cytokines, and GCAD in murine cardiac allografts. The effect of DDAH overexpression may be mediated by its reduction of plasma and tissue ADMA concentrations.
Overexpression of SOD1 attenuates both apoptosis and the inflammatory response during ischemia-reperfusion injury and therefore mitigates against the subsequent development of GCAD.
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