Kyushu University · 생화학·유전·분자생물학
동천 강 교수의 연구실은 미토콘드리아의 유전자 안정성과 손상 복구 메커니즘을 중심으로 연구를 진행하고 있습니다. 특히 미토콘드리아 내에서 산화적 손상으로 인한 DNA 손상 방지 기전, 8-oxo-dGTP 분해 효소(MTH1)의 세포 내 분포와 기능, TFAM 단백질이 미토콘드리아 DNA의 전사, 복제, 손상 감지 및 수리에 미치는 다각적 역할을 규명하고자 합니다. 또한 노화와 관련된 미토콘드리아 DNA 변이의 축적과 심장질환, 당뇨, 암 등 흔한 질환과의 연관성에 초점을 맞추고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
We examined the intracellular distribution of 8-oxo-dGTPase (8-oxo-7,8-dihydrodeoxyguanosine triphosphatase) encoded by the MTH1 gene, a human mutator homologue. The activity of 8-oxo-dGTPase mainly located in cytosolic and mitochondrial soluble fractions of Jurkat cells, a human T-cell leukemia line. Electron microscopic immunocytochemistry, using a specific antibody against MTH1 protein, showed localization of MTH1 protein in the mitochondrial matrix. Activity in the mitochondria accounted for
Mitochondria produce reactive oxygen species (ROS) under physiological conditions in association with activity of the respiratory chain in aerobic ATP production. The production of ROS is essentially a function of O2 consumption. Hence, increased mitochondrial activity per se can be an oxidative stress to cells. Furthermore, production of ROS is markedly enhanced in many pathological conditions in which the respiratory chain is impaired. Because mitochondrial DNA, which is essential for executio
It has long been considered that mitochondrial DNA disease is a rare genetic disorder causing neuromyopathy. However, alterations of mitochondrial DNA recently have been recognized to play an important role in the pathogenesis of so-called common diseases such as heart failure, diabetes, and cancer. Although some of these alterations are inherited, more and more attention is being focused on the accumulation of mitochondrial DNA mutations in somatic cells, particularly terminally differentiated
Mitochondria have their own genome, which is essential for proper oxidative phosphorylation needed for a large part of ATP production in a cell. Although mitochondrial DNA-less (rho0) cells can survive under special conditions, the integrity of the mitochondrial genome is critical for survival of multicellular organisms. Mitochondrial transcription factor A (TFAM), originally cloned as transcription factor, is essential for the maintenance of mtDNA. Recently, it has become known that TFAM plays
A large part of replication is aborted in human mitochondria, the result being a D-loop. As few attempts have been made to distinguish free 5' ends of true replicate from those of abortive ones, we examined the 5' ends of true replicate of human mitochondrial DNA at one nucleotide resolution in vivo by making use of ligation-mediated polymerase chain reaction. The distribution and relative amounts of origins of the true replicate are exactly the same as those of total newly synthesized heavy str
