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Kimiko Inoue
National Institutes of Health
18Publications
10H-index
1,920Citations
Publications 15
Newest
#2Shoji MaenoharaH-Index: 1
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#1Atsuo OguraH-Index: 60
#2Kimiko InoueH-Index: 10
Last.Teruhiko WakayamaH-Index: 58
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#1Atsuo OguraH-Index: 60
#2Kimiko InoueH-Index: 10
Last.Hiromi MikiH-Index: 31
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Source
#1Takashi Kohda (TITech: Tokyo Institute of Technology)H-Index: 31
#2Jiyoung Lee (TITech: Tokyo Institute of Technology)H-Index: 41
Last.Fumitoshi Ishino (TITech: Tokyo Institute of Technology)H-Index: 41
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Abstract Although somatic cell cloning has been accomplished in several mammalian species, its efficiency remains considerably low due to fetal mortality during the pre- and perinatal periods, which suggests incomplete initialization of epigenetic memories during the somatic cloning procedure. Genomic imprinting is an epigenetic mechanism that produces functional differences between the paternal and maternal genomes, and plays an essential role in mammalian development and growth. Therefore, it ...
Source
#1Narumi Ogonuki (NIH: National Institutes of Health)H-Index: 42
#2Kimiko Inoue (NIH: National Institutes of Health)H-Index: 10
Last.Atsuo Ogura (NIH: National Institutes of Health)H-Index: 60
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Here we report that the lifespan of mice cloned from somatic cells is significantly shorter than that of genotype- and sex-matched controls, most likely due to severe pneumonia and hepatic failure. This finding demonstrates the possibility of long-term deleterious effects of somatic-cell cloning, even after normal birth.
214 CitationsSource
#1Atsuo OguraH-Index: 60
#2Narumi OgonukiH-Index: 42
Last.Kimiko InoueH-Index: 10
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Publisher Summary This chapter focuses on microinsemination techniques using spermatozoa, spermatids, and spermatocytes, and on nuclear transfer techniques using male primordial germ cells. Microinsemination generally refers to intracytoplasmic sperm injection (ICSI) in which a sperm cell is injected directly into the cytoplasm of an oocyte, although it also includes techniques such as partial zona dissection and subzonal insemination that aid the passage of spermatozoa through the zona pellucid...
Source
#1Atsuo Ogura (NIH: National Institutes of Health)H-Index: 60
#2Narumi Ogonuki (NIH: National Institutes of Health)H-Index: 42
Last.Kimiko Inoue (NIH: National Institutes of Health)H-Index: 10
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23 CitationsSource
#1Kazuto Nakada (University of Tsukuba)H-Index: 30
#2Kimiko Inoue (NIH: National Institutes of Health)H-Index: 10
Last.Jun-Ichi Hayashi (University of Tsukuba)H-Index: 39
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We examined the correlation of functional and structural abnormalities of cardiac mitochondria created by pathogenic mutant mtDNAs using mito-mice with hearts carrying 88% mutant ΔmtDNA4696 with a 4696 deletion. COX histochemistry, quantitative PCR analysis, and electronmicrographs showed that accumulation of 91.6% ΔmtDNA4696 in single cardiac muscle fibers induced progressive reduction of COX activity to form COX-negative fibers. Moreover, hearts carrying 88% ΔmtDNA4696 consisted of three types...
19 CitationsSource
#1Kazuto Nakada (University of Tsukuba)H-Index: 30
#2Kimiko Inoue (NIH: National Institutes of Health)H-Index: 10
Last.Jun-Ichi Hayashi (University of Tsukuba)H-Index: 39
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Abstract We generated mice with deletion mutant mtDNA by its introduction from somatic cells into mouse zygotes. Expressions of disease phenotypes are limited to tissues expressing mitochondrial dysfunction. Considering that all these mice share the same nuclear background, these observations suggest that accumulation of the mutant mtDNA and resultant expressions of mitochondrial dysfunction are responsible for expression of disease phenotypes. On the other hand, mitochondrial dysfunction and ex...
38 CitationsSource
#1Kazuto Nakada (University of Tsukuba)H-Index: 30
#2Kimiko Inoue (University of Tsukuba)H-Index: 10
Last.Jun-Ichi Hayashi (University of Tsukuba)H-Index: 39
view all 8 authors...
Here we investigated the pathogenesis of deletion mutant mitochondrial (mt)DNA by generating mice with mutant mtDNA carrying a 4696-basepair deletion (ΔmtDNA4696), and by using cytochrome c oxidase (COX) electron micrographs to identify COX activity at the individual mitochondrial level. All mitochondria in tissues with ΔmtDNA4696 showed normal COX activity until ΔmtDNA4696 accumulated predominantly; this prevented mice from expressing disease phenotypes. Moreover, we did not observe coexistence...
325 CitationsSource
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