名古屋大学 · 医学
田中正史教授の研究室は、放射線や酸化的なストレスに対する極限環境に適応する微生物、特にデュラバクテルス・ラジオデュランスの応答機構を分子遺伝学的・ゲノムスケールで解明しています。特に、放射線や乾燥ストレスに起因するDNA損傷に対する応答に関与する遺伝子群（ddrA〜D、pprAなど）の機能と相互作用を解析しており、細胞の修復メカニズムの理解を深めています。また、心臓移植における炎症や酸化的損傷の抑制に寄与するD-アミノ酸化酵素（DDAH-I）やスーパーオキシドディスムターゼ（SOD1）の発現が、移植後の障害を軽減するメカニズムの解明にも貢献しています。
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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