Zobrazeno 1 - 10
of 11
pro vyhledávání: '"Hirotake Imanishi"'
Autor:
Takayuki Mito, Yoshiaki Kikkawa, Akinori Shimizu, Osamu Hashizume, Shun Katada, Hirotake Imanishi, Azusa Ota, Yukina Kato, Kazuto Nakada, Jun-Ichi Hayashi
Publikováno v:
PLoS ONE, Vol 8, Iss 2, p e55789 (2013)
Mitochondrial DNA (mtDNA) mutator mice are proposed to express premature aging phenotypes including kyphosis and hair loss (alopecia) due to their carrying a nuclear-encoded mtDNA polymerase with a defective proofreading function, which causes accele
Externí odkaz:
https://doaj.org/article/26e751ffb9a34aad969369972af64f56
Autor:
Hirotake Imanishi, Gaku Takibuchi, Toshihiko Kobayashi, Kaori Ishikawa, Kazuto Nakada, Masayuki Mori, Yoshiaki Kikkawa, Keizo Takenaga, Noriko Toyama-Sorimachi, Jun-Ichi Hayashi
Publikováno v:
PLoS ONE, Vol 8, Iss 9, p e75981 (2013)
In mammalian species, mitochondrial DNA (mtDNA) with pathogenic mutations that induce mitochondrial respiration defects has been proposed to be involved in tumor phenotypes via induction of enhanced glycolysis under normoxic conditions (the Warburg e
Externí odkaz:
https://doaj.org/article/3f956d1b06b14a1ea8aabea631650e76
Autor:
Hirotake Imanishi, Keisuke Hattori, Reiko Wada, Kaori Ishikawa, Sayaka Fukuda, Keizo Takenaga, Kazuto Nakada, Jun-ichi Hayashi
Publikováno v:
PLoS ONE, Vol 6, Iss 8, p e23401 (2011)
Mutations in mitochondrial DNA (mtDNA) might contribute to expression of the tumor phenotypes, such as metastatic potential, as well as to aging phenotypes and to clinical phenotypes of mitochondrial diseases by induction of mitochondrial respiration
Externí odkaz:
https://doaj.org/article/e48ab5ea89ea426abd8f6f6c11e142d6
Autor:
Hitoshi Suzuki, Kazuto Nakada, Chisato Hayashi, Shunkei Enoki, Hirotake Imanishi, Tetsuo Hashimoto, Akinori Shimizu, Kazuyuki Mekada, Jun-Ichi Hayashi, Osamu Hashizume
Publikováno v:
Experimental Animals
Previous reports have shown that transmitochondrial mito-mice with nuclear DNA from Mus musculus and mtDNA from M. spretus do not express respiration defects, whereas those with mtDNA from Rattus norvegicus cannot be generated from ES cybrids with mt
Publikováno v:
Journal of Bioenergetics and Biomembranes. 44:639-644
It has been controversial whether mtDNA mutations are responsible for tumorigenesis and for the process to develop metastases. To clarify this issue, we established trans-mitochondrial cybrids with mtDNA exchanged between mouse tumor cells that posse
Autor:
Jun-Ichi Hayashi, Kazuto Nakada, Masayuki Mori, Hirotake Imanishi, Akinori Shimizu, Mutsumi Yokota
Publikováno v:
Experimental Animals. 60:397-404
This study determined pathogenicity of an A11181G mtDNA mutation found in a senescence-accelerated mouse strain, SAMP8. The mutation was at a highly conserved site of the mt-Nd4 gene, which encodes one of the respiratory complex I subunits. The young
Autor:
Jun-Ichi Hayashi, Hiromichi Yonekawa, Hirotake Imanishi, Kaori Ishikawa, Keizo Takenaga, Noriko Toyama-Sorimachi, Shigemi Sasawatari, Mamoru Niikura, Mariko Yoshizaki, Mami Morimoto, Kazuto Nakada
Publikováno v:
The Journal of Experimental Medicine
Tumors or embryonic stem cells bearing foreign mitochondrial DNA are rejected by the innate immune system via a mechanism that depends on MyD88.
Mitochondrial DNA (mtDNA) has been proposed to be involved in respiratory function, and mtDNA mutati
Mitochondrial DNA (mtDNA) has been proposed to be involved in respiratory function, and mtDNA mutati
Autor:
Nobuko Koshikawa, Aya Yamaguchi, Keizo Takenaga, Hirotake Imanishi, Yoshio Honma, Miho Akimoto, Kazuto Nakada, Jun-Ichi Hayashi, Kaori Ishikawa
Publikováno v:
Science. 320:661-664
Mutations in mitochondrial DNA (mtDNA) occur at high frequency in human tumors, but whether these mutations alter tumor cell behavior has been unclear. We used cytoplasmic hybrid (cybrid) technology to replace the endogenous mtDNA in a mouse tumor ce
Autor:
Kaori Ishikawa, Gaku Takibuchi, Kazuto Nakada, Toshihiko Kobayashi, Jun-Ichi Hayashi, Noriko Toyama-Sorimachi, Yoshiaki Kikkawa, Masayuki Mori, Hirotake Imanishi, Keizo Takenaga
Publikováno v:
PLoS ONE
PLoS ONE, Vol 8, Iss 9, p e75981 (2013)
PLoS ONE, Vol 8, Iss 9, p e75981 (2013)
mammalian species, mitochondrial DNA (mtDNA) with pathogenic mutations that induce mitochondrial respiration defects has been proposed to be involved in tumor phenotypes via induction of enhanced glycolysis under normoxic conditions (the Warburg effe
Autor:
Yoshiaki Kikkawa, Akinori Shimizu, Shun Katada, Jun-Ichi Hayashi, Takayuki Mito, Hirotake Imanishi, Osamu Hashizume, Yukina Kato, Kazuto Nakada, Azusa Ota
Publikováno v:
PLoS ONE
PLoS ONE, Vol 8, Iss 2, p e55789 (2013)
PLoS ONE, Vol 8, Iss 2, p e55789 (2013)
Mitochondrial DNA (mtDNA) mutator mice are proposed to express premature aging phenotypes including kyphosis and hair loss (alopecia) due to their carrying a nuclear-encoded mtDNA polymerase with a defective proofreading function, which causes accele