Nagoya University · 의학
마사시 타나카 교수의 연구실은 DNA 복구 메커니즘과 산화적 스트레스에 대한 세포의 내성을 규명하는 데 초점을 맞추고 있습니다. 특히, 데르마토퓨스 라디오두르스의 방사선 내성과 탈수 스트레스 반응을 유전자 수준에서 분석하며, 이와 관련된 ddr 및 SOD1, DDAH-I 유전자 기능을 규명하고 있습니다. 또한, 심장 이식 및 심부전과 같은 질병 모델에서 산화 스트레스와 염증 반응을 조절하는 유전자 발현의 영향을 연구하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
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.
