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Kazuto Nakada
University of Tsukuba
97Publications
30H-index
4,012Citations
Publications 97
Newest
In a previous study, we proposed that age-related mitochondrial respiration defects observed in elderly subjects are partially due to age-associated downregulation of nuclear-encoded genes, including serine hydroxymethyltransferase 2 (SHMT2), which is involved in mitochondrial one-carbon (1C) metabolism. This assertion is supported by evidence that the disruption of mouse Shmt2 induces mitochondrial respiration defects in mouse embryonic fibroblasts generated from Shmt2-knockout E13.5 embryos ex...
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#1Emi Ogasawara (University of Tsukuba)H-Index: 6
#2Kazuto Nakada (University of Tsukuba)H-Index: 30
Last.Jun-Ichi Hayashi (University of Tsukuba)H-Index: 39
view all 5 authors...
Marked accumulation of mitochondrial DNA (mtDNA) with a particular pathogenic mutation is necessary for the mutant mtDNA to express its pathogenicity as mitochondrial respiration defects. However, the nuclear genome background, or the physiological status, or both, might also be important for the pathogenic regulation of mutant mtDNAs, because most mitochondrial function is controlled by polypeptides encoded in the nuclear genome. To test this, we generated diabetic mice carrying pathogenic mtDN...
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#1Kaori Ishikawa (University of Tsukuba)H-Index: 14
#2Kohei Kobayashi (University of Tsukuba)
Last.Kazuto Nakada (University of Tsukuba)H-Index: 30
view all 6 authors...
Accumulation of mutations in mitochondrial DNA (mtDNA) is thought to be responsible for mitochondrial, and other, diseases and biological phenomena, such as diabetes, cancer, neurodegenerative diseases, and aging. Mouse models may elucidate the relationship between mutations in mtDNA and these abnormalities. However, because of the difficulty of mtDNA manipulation, generation of mouse models has not sufficiently progressed to enable such studies. To overcome this difficulty and to establish a so...
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#1Kaori Ishikawa (University of Tsukuba)H-Index: 14
#2Satoshi Yamamoto (Takeda Pharmaceutical Company)H-Index: 2
Last.Kazuto Nakada (University of Tsukuba)H-Index: 30
view all 8 authors...
Neurons have high plasticity in developmental and juvenile stages that decreases in adulthood. Mitochondrial dynamics are highly important in neurons to maintain normal function. To compare dependency on mitochondrial dynamics in juvenile and adult stages, we generated a mouse model capable of selective timing of the expression of a mutant of the mitochondrial fusion factor Mitofusin 2 ( MFN2 ). Mutant expression in the juvenile stage had lethal effects. Contrastingly, abnormalities did not mani...
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#1Haruna Tani (University of Tsukuba)H-Index: 1
#2Sakiko Ohnishi (University of Tsukuba)H-Index: 2
Last.Jun-Ichi Hayashi (University of Tsukuba)H-Index: 39
view all 10 authors...
Accumulation of somatic mutations in mitochondrial DNA (mtDNA) has been proposed to be responsible for human aging and age-associated mitochondrial respiration defects. However, our previous findings suggested an alternative hypothesis of human aging—that epigenetic changes but not mutations regulate age-associated mitochondrial respiration defects, and that epigenetic downregulation of nuclear-coded genes responsible for mitochondrial translation [e.g., glycine C-acetyltransferase (GCAT), serin...
5 CitationsSource
#1Takayuki Mito (University of Tsukuba)H-Index: 5
#2Haruna Tani (University of Tsukuba)H-Index: 1
Last.Jun-Ichi Hayashi (University of Tsukuba)H-Index: 39
view all 6 authors...
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#1Tomoharu Yoshizumi (Kyushu University)H-Index: 34
#2Hiromi Imamura (Kyoto University)H-Index: 30
Last.Takumi Koshiba (Kyushu University)H-Index: 21
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Mitochondria act as a platform for antiviral innate immunity, and the immune system depends on activation of the retinoic acid-inducible gene I (RIG-I)-like receptors (RLR) signaling pathway via an adaptor molecule, mitochondrial antiviral signaling. We report that RLR-mediated antiviral innate immunity requires oxidative phosphorylation (OXPHOS) activity, a prominent physiologic function of mitochondria. Cells lacking mitochondrial DNA or mutant cells with respiratory defects exhibited severely...
9 CitationsSource
#1Akinori Shimizu (Fukuoka University)H-Index: 5
#2Haruna Tani (University of Tsukuba)H-Index: 1
Last.Jun-Ichi Hayashi (University of Tsukuba)H-Index: 39
view all 10 authors...
Abstract In a previous study, we generated transmitochondrial P29mtSAMP1 cybrids, which had nuclear DNA from the C57BL6 (referred to as B6) mouse strain-derived P29 tumor cells and mitochondrial DNA (mtDNA) exogenously-transferred from the allogeneic strain SAMP1. Because P29mtSAMP1 cybrids did not form tumors in syngeneic B6 mice, we proposed that allogeneic SAMP1 mtDNA suppressed tumor formation of P29mtSAMP1 cybrids. To test this hypothesis, current study generated P29mt(sp)B6 cybrids carryin...
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#2Fumika KoyanoH-Index: 9
Last.Noriyuki MatsudaH-Index: 22
view all 6 authors...
#1Tetsuro Matsuhashi (Tohoku University)H-Index: 6
#2Takeya Sato (Tohoku University)H-Index: 13
Last.Takaaki Abe (Tohoku University)H-Index: 41
view all 41 authors...
Abstract Mitochondrial dysfunction increases oxidative stress and depletes ATP in a variety of disorders. Several antioxidant therapies and drugs affecting mitochondrial biogenesis are undergoing investigation, although not all of them have demonstrated favorable effects in the clinic. We recently reported a therapeutic mitochondrial drug mitochonic acid MA-5 (Tohoku J. Exp. Med., 2015). MA-5 increased ATP, rescued mitochondrial disease fibroblasts and prolonged the life span of the disease mode...
10 CitationsSource
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