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Funako 1737, Atsugi, Kanagawa, Japan |
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KURAMOTO Takashi Professor |
From Graduate School 【 display / non-display 】
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Kyoto University Graduate School, Division of Medicine Doctor Course Accomplished credits for doctoral program
1993.04 - 1997.03
Country：Japan
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Kyoto University Graduate School, Division of Agriculture Master Course Completed
1990.04 - 1992.03
Country：Japan
Employment Record in Research 【 display / non-display 】
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Tokyo University of Agriculture Faculty of Agriculture Department of Animal Science Professor
2018.04
Research Interests 【 display / non-display 】
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experimental animals
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rat
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disease model
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polled gene
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A2 milk
Papers 【 display / non-display 】
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KUNISAWA Naofumi, OHNO Yukihiro, SHIMIZU Saki, KUWAMURA Mitsuru, SERIKAWA Tadao, IZAWA Takeshi, TANAKA Miyuu, YAMATE Jyoji, KURAMOTO Takashi, NUMAKURA Yuki
Experimental Animals advpub ( 0 ) 2026
Language：English Publisher：Japanese Association for Laboratory Animal Science
<p>Noda epileptic rat (NER) is a mutant model for epilepsy that exhibits spontaneous generalized tonic-clonic seizure. Epileptogenesis of NER remains to be elucidated; but it is detected an insertion of an endogenous retrovirus sequence in intron 2 of the PHD finger protein 24 (<i>Phf24</i>) gene. PHF24 is widely expressed in the soma of neurons and neuropil in the wild-type rat brain and spinal cord but significantly less expressed in NER. In addition, the characteristic PHF24 expressions were noted in the soma of specific populations of the inhibitory interneurons. Here, we first examined the morphology of the neurons and synapses in the brain of NER to evaluate the epileptogenesis of NER. In NER, the total number of neurons was decreased, but the inhibitory neurons were increased. Inhibitory synapses increased while excitatory synapses tended to decrease in NER. Secondary, we examined <i>Phf24</i>-null rat without symptom of seizures in the same manner and evaluate a contribution of PHF24 to the epileptogeneis of NER. Interestingly, the opposite trend was observed in <i>Phf24</i>-null rats, with a decrease in the inhibitory neurons and synapses, an increase trend in the excitatory synapses. PHF24 is considered to play an important role in maintaining of the inhibitory neurons in the rat brain. We conclude that the reduction of PHF24 might lead to impaired inhibitory signals and increase susceptibility to epilepsy in NER. The histopathological changes of NER in the present study may represent a secondary change to repeated seizures.</p>
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A nonsense mutation in the <i>Mocos</i> gene induces xanthinuria, obstructive nephropathy, and anemia in rats
URASAKI Mao, NAGASAKA Kana, KIDO Minori, HAYASHI Kenta, WATANABE Ayumi, HATTORI Kosuke, SEKIGUCHI Takahiro, KUWAMURA Mitsuru, TANAKA Miyuu, MASHIMO Tomoji, KURAMOTO Takashi
Experimental Animals advpub ( 0 ) 2025
Language：English Publisher：Japanese Association for Laboratory Animal Science
<p>Xanthinuria type II is a rare hereditary disorder caused by mutations in the <i>MOCOS</i> gene, leading to dual deficiency of xanthine dehydrogenase and aldehyde oxidase. To establish a robust animal model for this condition, we generated <i>Mocos</i> knock-in (KI) rats carrying the Arg419Ter nonsense mutation identified in Japanese patients. Homozygous KI rats exhibited severe growth retardation, anemia, and reduced survival, with all individuals dying by 14 weeks of age. Biochemical analyses revealed elevated levels of hypoxanthine and xanthine, along with decreased uric acid in both serum and urine, confirming xanthinuria. Homozygous KI rats also showed increased blood creatinine (CRE) and urea nitrogen (UN), and decreased urinary CRE and UN, indicating renal dysfunction. Histopathological examination showed obstructive nephropathy characterized by tubular atrophy, crystal deposition, and inflammation. Compared to existing mouse models, <i>Mocos</i> KI rats demonstrated extended lifespan, enabling more detailed investigation of disease mechanisms. This rat model provides a valuable tool for studying the pathogenesis of xanthinuria type II and exploring potential therapeutic strategies.</p>
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A nonsense mutation in the <i>Mocos</i> gene induces xanthinuria, obstructive nephropathy, and anemia in rats
URASAKI Mao, NAGASAKA Kana, KIDO Minori, HAYASHI Kenta, WATANABE Ayumi, HATTORI Kosuke, SEKIGUCHI Takahiro, KUWAMURA Mitsuru, TANAKA Miyuu, MASHIMO Tomoji, KURAMOTO Takashi
Experimental Animals advpub ( 0 ) 2025
Language：English Publisher：Japanese Association for Laboratory Animal Science
<p>Xanthinuria type II is a rare hereditary disorder caused by mutations in the <i>MOCOS</i> gene, leading to dual deficiency of xanthine dehydrogenase and aldehyde oxidase. To establish a robust animal model for this condition, we generated <i>Mocos</i> knock-in (KI) rats carrying the Arg419Ter nonsense mutation identified in Japanese patients. Homozygous KI rats exhibited severe growth retardation, anemia, and reduced survival, with all individuals dying by 14 weeks of age. Biochemical analyses revealed elevated levels of hypoxanthine and xanthine, along with decreased uric acid in both serum and urine, confirming xanthinuria. Homozygous KI rats also showed increased blood creatinine (CRE) and urea nitrogen (UN), and decreased urinary CRE and UN, indicating renal dysfunction. Histopathological examination showed obstructive nephropathy characterized by tubular atrophy, crystal deposition, and inflammation. Compared to existing mouse models, <i>Mocos</i> KI rats demonstrated extended lifespan, enabling more detailed investigation of disease mechanisms. This rat model provides a valuable tool for studying the pathogenesis of xanthinuria type II and exploring potential therapeutic strategies.</p>
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HIEU Hoang Trung, TANAKA Miyuu, KUWAMURA Mitsuru, MASHIMO Tomoji, SERIKAWA Tadao, KURAMOTO Takashi
Experimental Animals advpub ( 0 ) 88 - 94 2022
Language：English Publisher：Japanese Association for Laboratory Animal Science
<p>Rodent coat color genes have been studied as a bioresource to understand developmental and cellular processes. The Downunder rat is a fancy variety with a marking on its belly that runs from the neck to the breech and appears to mirror the dorsal hooded marking. Here, we established a congenic strain carrying the Downunder (<i>Du</i>) gene in an F344 genetic background. In addition to the ventral marking, <i>Du</i>/+ rats exhibit anophthalmia or microphthalmia with incomplete penetrance. <i>Du</i>/<i>Du</i> embryos die in the early stages of organogenesis. Genetic linkage analysis mapped the <i>Du</i> gene to rat chromosome 3 and haplotype mapping with congenic rats localized the <i>Du</i> locus to a 3.9-Mb region. The <i>Du</i> locus includes two functional genes, glycosyltransferase-like domain-containing 1 (<i>Gtdc1</i>) and zinc finger E-box binding homeobox 2 (<i>Zeb2</i>). Although we found no functional variation within any of <i>Zeb2</i>’s exons or intron-exon boundaries, <i>Zeb2</i> mRNA levels were significantly lower in <i>Du</i>/+ rats compared with wild-type rats. It is known that melanocyte-specific <i>Zeb2</i> deletion results in the congenital loss of hair pigmentation in mice. Taken together, our results indicate that the <i>Du</i> mutation exerts pleiotropic effects on hair pigmentation, eye morphology, and development. Moreover, the <i>Zeb2</i> gene is a strong candidate for the <i>Du</i> mutation.</p>
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Positional cloning of rat mutant genes reveals new functions of these genes
KURAMOTO Takashi
Experimental Animals advpub ( 0 ) 1 - 8 2022
Language：English Publisher：Japanese Association for Laboratory Animal Science
<p>The laboratory rat (<i>Rattus norvegicus</i>) is a key model organism for biomedical research. Rats can be subjected to strict genetic and environmental controls. The rat’s large body size is suitable for both surgical operations and repeated measurements of physiological parameters. These advantages have led to the development of numerous rat models for genetic diseases. Forward genetics is a proven approach for identifying the causative genes of these disease models but requires genome resources including genetic markers and genome sequences. Over the last few decades, rat genome resources have been developed and deposited in bioresource centers, which have enabled us to perform positional cloning in rats. To date, more than 100 disease-related genes have been identified by positional cloning. Since some disease models are more accessible in rats than mice, the identification of causative genes in these models has sometimes led to the discovery of novel functions of genes. As before, various mutant rats are also expected to be discovered and developed as disease models in the future. Thus, the forward genetics continues to be an important approach to find genes involved in disease phenotypes in rats. In this review, I provide an overview the development of rat genome resources and describe examples of positional cloning in rats in which novel gene functions have been identified.</p>
Books and Other Publications 【 display / non-display 】
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ストーリーで惹きつける科学プレゼンテーション法 : 魅力的かつ論理的に自身の研究成果を伝える世界標準のフォーマット
Kirchoff Bruce, 庫本 高志, Wagner Jon illustrator
羊土社 2023 （ ISBN:9784758108553 ）
Language：Japanese
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マウス・ラット実験ノート : はじめての取り扱い、倫理・法的規制から、飼育法・投与・麻酔・解剖、分子生物学的手法とゲノム編集まで
北田 一博, 庫本 高志, 真下 知士 , 中釜 斉
羊土社 2023 （ ISBN:9784758122627 ）
Language：Japanese
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Basic Laboratory Animal Science and Technology, Expanded and Revised Edition
（ Role： Joint editor）
2021.04
Language：Japanese Book type：Scholarly book
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Advanced Laboratory Animal Science and Technology, Expanded and Revised Edition
（ Role： Joint editor）
2021.04
Language：Japanese Book type：Scholarly book
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特集 実験動物としてのラットの有用性 連載にあたって LABIO21 No.78: p12
庫本高志（ Role： Sole author）
日本実験動物協会 2019.10
Language：Japanese Book type：Scholarly book
Honours, Awards and Prizes 【 display / non-display 】
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公益社団法人 日本実験動物学会 学会賞安東・田嶋賞
2022.05
Award type：International academic award (Japan or overseas) Country：Japan
Presentations 【 display / non-display 】
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Enhanced sensitivity of epileptic seizure by deficit of hyperpolarization activated cyclic nucleotide-gated (HCN) channel 1
Shimizu Saki, Ishizaki Yuto, Hattori Tatsuya, Kotaru Yuki, Mishio Sara, Kuramoto Takashi, Ohno Yukihiro
Proceedings for Annual Meeting of The Japanese Pharmacological Society 2022 Proceedings for Annual Meeting of The Japanese Pharmacological Society
Event date： 2022
Language：Japanese Presentation type：Oral presentation (general)
<p>Hyperpolarization activated cyclic nucleotide-gated (HCN) channels underlie hyperpolarization-activated current (<i>I</i><sub>h</sub>) generation, regulating spontaneous rhythm and neural oscillation. HCN1 channels are abundantly expressed in the cerebral cortex, hippocampus and brain stem and are suggested to be involved in the initiation and propagation of spontaneous generalized seizure, however, the functional mechanism is still unknown. In this study, to clarify the role of HCN1 channel in induction of epileptic seizure, we performed the chemically- and electrically-induced seizure tests using <i>Hcn1</i> knock-out (<i>Hcn1</i>-KO) rats. Pilocarpine and 4-aminopyridine produced significantly higher seizure induction in<i> Hcn1</i>-KO rats than in control (F344) rats. <i>Hcn1</i>-KO rats also showed higher sensitivity to electrical shock-induced seizures. In addition, we performed the immunohistochemical analysis of c-Fos expression following electrical shock-induced seizures. <i>Hcn1</i>-KO rats showed a significantly higher Fos expression than control rats in the cerebral cortex and amygdala. These results suggest that HCN1 channels play a crucial role in controlling the susceptibility to epileptic seizure, implying that hyperactivation of the cerebral cortex and amygdala is involved in the enhancement of seizure susceptibility due to loss of HCN1 channel.</p>
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The 3rd Term of the National BioResource Project-Rat in Japan Invited International conference
Kaneko T, Tanaka M, Taketsuru H, Voigt B, Neoda Y, Hagiwara K, Cui Z, Nakagawa Y, Nagao T, Nakanishi S, Yamasaki K, Kuramoto T
The 8th ANRRC Internatinal Meeting 2016.09 ANRRC（Asian Network of Research Resource Center)
Event date： 2016.09
Language：English Presentation type：Oral presentation (invited, special)
Venue：Shiran Kaikan, Kyoto University, Kyoto, Japan
アジアのバイオリソース関連機関の集会において、ナショナルバイオリソースプロジェクト「ラット」を紹介した。
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アトピー性皮膚炎モデルラットの治療試験
庫本高志、横江繭子、西谷あい、日合 弘、椛島健治
第63回日本実験動物学会 2016.05 日本実験動物学会
Event date： 2016.05
Language：Japanese Presentation type：Oral presentation (general)
Venue：ミューザ川崎シンフォニーホール(川崎市幸区)
アトピー性皮膚炎モデルラットを用いた皮膚炎の治療試験を報告した。
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TRM/Kyoラットにおける本態性振戦の原因遺伝子の解明
西谷あい、田中美有、清水佐紀、國澤直史、横江繭子、吉田裕作、鈴木登志郎、佐久間哲史、山本 卓、桑村 充、竹中重雄、大野行弘、庫本高志
第63回日本実験動物学会 2016.05 日本実験動物学会
Event date： 2016.05
Language：Japanese Presentation type：Oral presentation (general)
Venue：ミューザ川崎シンフォニーホール(川崎市幸区)
ラットモデルを用いて本態性振戦の原因遺伝子を同定した。
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新たなアトピー性皮膚炎モデルの開発
庫本高志、横江繭子、由利 梓、西谷あい、田中大資、日合 弘、芹川忠夫
第62回日本実験動物学会 2015.05 日本実験動物学会
Event date： 2015.05
Language：Japanese Presentation type：Oral presentation (general)
Venue：京都テルサ(京都市南区)
KFRS4ラットをアトピー性皮膚炎モデルとして開発した。
Committee Memberships 【 display / non-display 】
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日本実験動物学会 理事
2016.05 - 2022.05
Committee type：Academic society
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日本実験動物学会 評議員
2014.05
Committee type：Academic society