Search

Your search keyword '"Nakamura, Kazuomi"' showing total 35 results
Start Over Author "Nakamura, Kazuomi"
35 results on '"Nakamura, Kazuomi"'

17. Cover

Author

Nagira, Kei, primary, Taniguchi, Fuminori, additional, Nakamura, Kazuomi, additional, Tokita, Yohei, additional, Tsuchiya, Naoko, additional, Khine, Yin Mon, additional, and Harada, Tasuku, additional

Published
2019
Full Text
View/download PDF

22. Modification of single-nucleotide polymorphism in a fully humanized CYP3A mouse by genome editing technology

Author

Abe, Satoshi, primary, Kobayashi, Kaoru, additional, Oji, Asami, additional, Sakuma, Tetsushi, additional, Kazuki, Kanako, additional, Takehara, Shoko, additional, Nakamura, Kazuomi, additional, Okada, Azusa, additional, Tsukazaki, Yasuko, additional, Senda, Naoto, additional, Honma, Kazuhisa, additional, Yamamoto, Takashi, additional, Ikawa, Masahito, additional, Chiba, Kan, additional, Oshimura, Mitsuo, additional, and Kazuki, Yasuhiro, additional

Published
2017
Full Text
View/download PDF

24. Modification of single-nucleotide polymorphism in a fully humanized CYP3A mouse by genome editing technology

Author

Abe, Satoshi, 1000030255864, Kobayashi, Kaoru, 1000050803417, Oji, Asami, 1000090711143, Sakuma, Tetsushi, 1000000774043, Kazuki, Kanako, Takehara, Shoko, 1000090598137, Nakamura, Kazuomi, Okada, Azusa, Tsukazaki, Yasuko, Senda, Naoto, Honma, Kazuhisa, Yamamoto, Takashi, 1000020304066, Ikawa, Masahito, 1000040159033, Chiba, Kan, 1000020111619, Oshimura, Mitsuo, 1000090403401, Kazuki, Yasuhiro, Abe, Satoshi, 1000030255864, Kobayashi, Kaoru, 1000050803417, Oji, Asami, 1000090711143, Sakuma, Tetsushi, 1000000774043, Kazuki, Kanako, Takehara, Shoko, 1000090598137, Nakamura, Kazuomi, Okada, Azusa, Tsukazaki, Yasuko, Senda, Naoto, Honma, Kazuhisa, Yamamoto, Takashi, 1000020304066, Ikawa, Masahito, 1000040159033, Chiba, Kan, 1000020111619, Oshimura, Mitsuo, 1000090403401, and Kazuki, Yasuhiro

Abstract

Abe, S., Kobayashi, K., Oji, A. et al. Modification of single-nucleotide polymorphism in a fully humanized CYP3A mouse by genome editing technology. Sci Rep 7, 15189 (2017). https://doi.org/10.1038/s41598-017-15033-0, Cytochrome P450, family 3, subfamily A (CYP3A) enzymes metabolize approximately 50% of commercially available drugs. Recently, we developed fully humanized transchromosomic (Tc) CYP3A mice with the CYP3A cluster including CYP3A4, CYP3A5, CYP3A7, and CYP3A43. Our humanized CYP3A mice have the CYP3A5∗3 (g.6986G) allele, resulting in the almost absence of CYP3A5 protein expression in the liver and intestine. To produce model mice for predicting CYP3A5′s contribution to pharmacokinetics, we performed a single-nucleotide polymorphism (SNP) modification of CYP3A5 (g.6986G to A,∗3 to∗1) on the CYP3A cluster using genome editing in both mouse ES cells and fertilized eggs, and produced humanized CYP3A5∗1 mice recapitulating the CYP3A5∗1 carrier phenotype in humans. The humanized CYP3A mouse with CYP3A5∗1 is the first Tc mouse for predicting the SNP effect on pharmacokinetics in humans. The combination of Tc technology and genome editing enables the production of useful humanized models that reflect humans with different SNPs.

Published
2017

29. Use of a Human Artificial Chromosome for Delivering Trophic Factors in a Rodent Model of Amyotrophic Lateral Sclerosis

Author

Watanabe, Yasuhiro, primary, Kazuki, Yasuhiro, additional, Kazuki, Kanako, additional, Ebiki, Mitsutaka, additional, Nakanishi, Mami, additional, Nakamura, Kazuomi, additional, Yoshida Yamakawa, Miho, additional, Hosokawa, Hiroyuki, additional, Ohbayashi, Tetsuya, additional, Oshimura, Mitsuo, additional, and Nakashima, Kenji, additional

Published
2015
Full Text
View/download PDF

30. Repression of Cyclin D1 Expression Is Necessary for the Maintenance of Cell Cycle Exit in Adult Mammalian Cardiomyocytes

Author

Tane, Shoji, primary, Kubota, Misae, additional, Okayama, Hitomi, additional, Ikenishi, Aiko, additional, Yoshitome, Satoshi, additional, Iwamoto, Noriko, additional, Satoh, Yukio, additional, Kusakabe, Aoi, additional, Ogawa, Satoko, additional, Kanai, Ayumi, additional, Molkentin, Jeffery D., additional, Nakamura, Kazuomi, additional, Ohbayashi, Tetsuya, additional, and Takeuchi, Takashi, additional

Published
2014
Full Text
View/download PDF

31. Histone H3 lysine 9 methyltransferases, G9a and GLP are essential for cardiac morphogenesis

Author

Inagawa, Masayo, primary, Nakajima, Kuniko, additional, Makino, Tomoyuki, additional, Ogawa, Satoko, additional, Kojima, Mizuyo, additional, Ito, Satomi, additional, Ikenishi, Aiko, additional, Hayashi, Toshinori, additional, Schwartz, Robert J., additional, Nakamura, Kazuomi, additional, Obayashi, Tetsuya, additional, Tachibana, Makoto, additional, Shinkai, Yoichi, additional, Maeda, Kazuhiro, additional, Miyagawa-Tomita, Sachiko, additional, and Takeuchi, Takashi, additional

Published
2013
Full Text
View/download PDF

32. Modification of single-nucleotide polymorphism in a fully humanized CYP3A mouse by genome editing technology

Author

Abe, Satoshi, Kobayashi, Kaoru, Oji, Asami, Sakuma, Tetsushi, Kazuki, Kanako, Takehara, Shoko, Nakamura, Kazuomi, Okada, Azusa, Tsukazaki, Yasuko, Senda, Naoto, Honma, Kazuhisa, Yamamoto, Takashi, Ikawa, Masahito, Chiba, Kan, Oshimura, Mitsuo, Kazuki, Yasuhiro, Abe, Satoshi, Kobayashi, Kaoru, Oji, Asami, Sakuma, Tetsushi, Kazuki, Kanako, Takehara, Shoko, Nakamura, Kazuomi, Okada, Azusa, Tsukazaki, Yasuko, Senda, Naoto, Honma, Kazuhisa, Yamamoto, Takashi, Ikawa, Masahito, Chiba, Kan, Oshimura, Mitsuo, and Kazuki, Yasuhiro

Abstract

Cytochrome P450, family 3, subfamily A (CYP3A) enzymes metabolize approximately 50% of commercially available drugs. Recently, we developed fully humanized transchromosomic (Tc) CYP3A mice with the CYP3A cluster including CYP3A4, CYP3A5, CYP3A7, and CYP3A43. Our humanized CYP3A mice have the CYP3A5∗3 (g.6986G) allele, resulting in the almost absence of CYP3A5 protein expression in the liver and intestine. To produce model mice for predicting CYP3A5′s contribution to pharmacokinetics, we performed a single-nucleotide polymorphism (SNP) modification of CYP3A5 (g.6986G to A,∗3 to∗1) on the CYP3A cluster using genome editing in both mouse ES cells and fertilized eggs, and produced humanized CYP3A5∗1 mice recapitulating the CYP3A5∗1 carrier phenotype in humans. The humanized CYP3A mouse with CYP3A5∗1 is the first Tc mouse for predicting the SNP effect on pharmacokinetics in humans. The combination of Tc technology and genome editing enables the production of useful humanized models that reflect humans with different SNPs., Abe, S., Kobayashi, K., Oji, A. et al. Modification of single-nucleotide polymorphism in a fully humanized CYP3A mouse by genome editing technology. Sci Rep 7, 15189 (2017). https://doi.org/10.1038/s41598-017-15033-0

33. Modification of single-nucleotide polymorphism in a fully humanized CYP3A mouse by genome editing technology

Author

Abe, Satoshi, Kobayashi, Kaoru, Oji, Asami, Sakuma, Tetsushi, Kazuki, Kanako, Takehara, Shoko, Nakamura, Kazuomi, Okada, Azusa, Tsukazaki, Yasuko, Senda, Naoto, Honma, Kazuhisa, Yamamoto, Takashi, Ikawa, Masahito, Chiba, Kan, Oshimura, Mitsuo, Kazuki, Yasuhiro, Abe, Satoshi, Kobayashi, Kaoru, Oji, Asami, Sakuma, Tetsushi, Kazuki, Kanako, Takehara, Shoko, Nakamura, Kazuomi, Okada, Azusa, Tsukazaki, Yasuko, Senda, Naoto, Honma, Kazuhisa, Yamamoto, Takashi, Ikawa, Masahito, Chiba, Kan, Oshimura, Mitsuo, and Kazuki, Yasuhiro

Abstract

Abe, S., Kobayashi, K., Oji, A. et al. Modification of single-nucleotide polymorphism in a fully humanized CYP3A mouse by genome editing technology. Sci Rep 7, 15189 (2017). https://doi.org/10.1038/s41598-017-15033-0, Cytochrome P450, family 3, subfamily A (CYP3A) enzymes metabolize approximately 50% of commercially available drugs. Recently, we developed fully humanized transchromosomic (Tc) CYP3A mice with the CYP3A cluster including CYP3A4, CYP3A5, CYP3A7, and CYP3A43. Our humanized CYP3A mice have the CYP3A5∗3 (g.6986G) allele, resulting in the almost absence of CYP3A5 protein expression in the liver and intestine. To produce model mice for predicting CYP3A5′s contribution to pharmacokinetics, we performed a single-nucleotide polymorphism (SNP) modification of CYP3A5 (g.6986G to A,∗3 to∗1) on the CYP3A cluster using genome editing in both mouse ES cells and fertilized eggs, and produced humanized CYP3A5∗1 mice recapitulating the CYP3A5∗1 carrier phenotype in humans. The humanized CYP3A mouse with CYP3A5∗1 is the first Tc mouse for predicting the SNP effect on pharmacokinetics in humans. The combination of Tc technology and genome editing enables the production of useful humanized models that reflect humans with different SNPs.

34. Uromodulin Regulates Murine Aquaporin-2 Activity via Thick Ascending Limb-Collecting Duct Cross-Talk during Water Deprivation.

Author

Takata T, Hamada S, Mae Y, Iyama T, Ogihara R, Seno M, Nakamura K, Takata M, Sugihara T, and Isomoto H

Subjects
Animals, Mice, Water Deprivation, Aquaporin 2 genetics, Aquaporin 2 metabolism, Hypertension metabolism, Kidney Tubules, Collecting metabolism, Uromodulin metabolism
Abstract

Uromodulin, a urinary protein synthesized and secreted from the thick ascending limb (TAL) of the loop of Henle, is associated with hypertension through the activation of sodium reabsorption in the TAL. Uromodulin is a potential target for hypertension treatment via natriuresis. However, its biological function in epithelial cells of the distal nephron segment, particularly the collecting duct, remains unknown. Herein, we examined the regulation of uromodulin production during water deprivation in vivo as well as the effect of uromodulin on the activity of the water channel aquaporin-2 (AQP2) in vitro and in vivo using transgenic mice. Water deprivation upregulated uromodulin production; immunofluorescence experiments revealed uromodulin adhesion on the apical surface of the collecting duct. Furthermore, the activation of AQP2 was attenuated in mice lacking uromodulin. Uromodulin enhanced the phosphorylation and apical trafficking of AQP2 in mouse collecting duct cells treated with the vasopressin analog dDAVP. The uromodulin-induced apical trafficking of AQP2 was attenuated via endocytosis inhibitor treatment, suggesting that uromodulin activates AQP2 through the suppression of endocytosis. This study provides novel insights into the cross-talk between TAL and the collecting duct, and indicates that the modulation of uromodulin is a promising approach for diuresis and hypertension treatment.

Published
2022
Full Text
View/download PDF

35. Use of a Human Artificial Chromosome for Delivering Trophic Factors in a Rodent Model of Amyotrophic Lateral Sclerosis.

Author

Watanabe Y, Kazuki Y, Kazuki K, Ebiki M, Nakanishi M, Nakamura K, Yoshida Yamakawa M, Hosokawa H, Ohbayashi T, Oshimura M, and Nakashima K

Abstract

A human artificial chromosome (HAC) is maintained as an episome within a cell and avoids random integration into the host genome. It can transfer multiple and/or large transgenes along with their regulatory elements thereby resembling native chromosomes. Using this HAC system, we established mesenchymal stem cells (MSCs) that simultaneously expressed hepatocyte growth factor, glial cell line-derived neurotrophic factor, and insulin-like growth factor 1, termed HAC-MSCs. This cell line provides an opportunity for stable transplantation and thorough analyses. We then introduced the cells for the treatment of a neurodegenerative disorder, amyotrophic lateral sclerosis. The HAC-MSCs were transplanted via the fourth cerebral ventricle (CV) or intravenous (i.v.) infusion at various ages of recipient mice. Littermate- and sex-matched mice underwent a sham procedure. Compared to the controls, there was an encouraging trend of increased life span via CV transplantation and delayed onset in i.v. infusion 60 days after transplantation. Further, we confirmed a statistically significant increase in life span via CV transplantation at 100 days. This effect was not seen in mice transplanted with MSCs lacking the HAC. We successfully enhanced the trophic potential of the MSCs using the HAC. This strategy could be a promising direction for the treatment of neurodegenerative disorders.

Published
2015
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results