Updated on 2025/11/05

写真a

 
ODA Kanako
 
Organization
Brain Research Institute Center for Bioresources Assistant Professor
Title
Assistant Professor
External link

Degree

  • 博士(医学) ( 2014.3   新潟大学 )

Research Areas

  • Life Science / Developmental biology

Research History (researchmap)

  • Niigata University   Brain Research Institute Center for Bioresources Bioresource Science Branch Department of Comparative and Experimental Medicine

    2009.4

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  • 三菱化学生命科学研究所

    2005.4 - 2009.3

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Research History

  • Niigata University   Brain Research Institute Center for Bioresources   Assistant Professor

    2017.4

  • Niigata University   Brain Research Institute Center for Bioresources   Specially Appointed Assistant Professor

    2013.4 - 2017.3

Professional Memberships

 

Papers

  • Axonal mRNA binding of hnRNP A/B is crucial for axon targeting and maturation of olfactory sensory neurons Reviewed

    Nanaho Fukuda, Tomoyuki Fukuda, Piergiorgio Percipalle, Kanako Oda, Nobuyuki Takei, Kevin Czaplinski, Kazushige Touhara, Yoshihiro Yoshihara, Toshikuni Sasaoka

    Cell Reports   42 ( 5 )   112398 - 112398   2023.5

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    DOI: 10.1016/j.celrep.2023.112398

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  • Importance of the Q/N-rich segment for protein stability of endogenous mouse TDP-43. Reviewed International journal

    Toshiya Sato, Kanako Oda, Seiko Sakai, Rika Kato, Saori Yamamori, Makoto Itakura, Yoshio Kodera, Masatoyo Nishizawa, Toshikuni Sasaoka, Osamu Onodera, Minesuke Yokoyama

    Scientific reports   12 ( 1 )   14923 - 14923   2022.9

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    TAR DNA-binding protein 43 kDa (TDP-43), a nuclear protein, plays an important role in the molecular pathogenesis of amyotrophic lateral sclerosis (ALS). The long-disordered C-terminal region (CTR) of TDP-43 is known to be aggregation-prone and a hotspot for ALS mutations, so elucidation of the physiological function of CTR will provide insights into the pathogenesis of ALS. The CTR has two Gly, aromatic, and Ser-rich (GaroS) segments and an amyloidogenic core divided into a hydrophobic patch (HP) and a Gln/Asn (Q/N)-rich segment. Although TDP-43 lacking the CTR is known to be unstable, as observed in knock-in mice, it is unclear which of these segments contributes to the stability of TDP-43. Here, we generated 12 mouse lines lacking the various sub-regions of CTR by genome editing and compared the embryonic lethality of homozygotes, and protein and mRNA expression levels of TDP-43. We demonstrated the functional diversity of the four segments of CTR, finding that the presence of the Q/N-rich segment greatly restored the protein stability of TDP-43. In addition, we found that the second GaroS deletion did not affect protein stability and mouse development.

    DOI: 10.1038/s41598-022-19153-0

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  • Brown adipose tissue dysfunction promotes heart failure via a trimethylamine N-oxide-dependent mechanism. Reviewed International journal

    Yohko Yoshida, Ippei Shimizu, Atsuhiro Shimada, Keita Nakahara, Sachiko Yanagisawa, Minoru Kubo, Shinji Fukuda, Chiharu Ishii, Hiromitsu Yamamoto, Takamasa Ishikawa, Kuniyuki Kano, Junken Aoki, Goro Katsuumi, Masayoshi Suda, Kazuyuki Ozaki, Yutaka Yoshida, Shujiro Okuda, Shigeo Ohta, Shiki Okamoto, Yasuhiko Minokoshi, Kanako Oda, Toshikuni Sasaoka, Manabu Abe, Kenji Sakimura, Yoshiaki Kubota, Norihiko Yoshimura, Shingo Kajimura, Maria Zuriaga, Kenneth Walsh, Tomoyoshi Soga, Tohru Minamino

    Scientific reports   12 ( 1 )   14883 - 14883   2022.9

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    Low body temperature predicts a poor outcome in patients with heart failure, but the underlying pathological mechanisms and implications are largely unknown. Brown adipose tissue (BAT) was initially characterised as a thermogenic organ, and recent studies have suggested it plays a crucial role in maintaining systemic metabolic health. While these reports suggest a potential link between BAT and heart failure, the potential role of BAT dysfunction in heart failure has not been investigated. Here, we demonstrate that alteration of BAT function contributes to development of heart failure through disorientation in choline metabolism. Thoracic aortic constriction (TAC) or myocardial infarction (MI) reduced the thermogenic capacity of BAT in mice, leading to significant reduction of body temperature with cold exposure. BAT became hypoxic with TAC or MI, and hypoxic stress induced apoptosis of brown adipocytes. Enhancement of BAT function improved thermogenesis and cardiac function in TAC mice. Conversely, systolic function was impaired in a mouse model of genetic BAT dysfunction, in association with a low survival rate after TAC. Metabolomic analysis showed that reduced BAT thermogenesis was associated with elevation of plasma trimethylamine N-oxide (TMAO) levels. Administration of TMAO to mice led to significant reduction of phosphocreatine and ATP levels in cardiac tissue via suppression of mitochondrial complex IV activity. Genetic or pharmacological inhibition of flavin-containing monooxygenase reduced the plasma TMAO level in mice, and improved cardiac dysfunction in animals with left ventricular pressure overload. In patients with dilated cardiomyopathy, body temperature was low along with elevation of plasma choline and TMAO levels. These results suggest that maintenance of BAT homeostasis and reducing TMAO production could be potential next-generation therapies for heart failure.

    DOI: 10.1038/s41598-022-19245-x

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  • Generation of Lungs by Blastocyst Complementation in Apneumic Fgf10-Deficient Mice Reviewed International journal

    Akihiko Kitahara, Qingsong Ran, Kanako Oda, Akihiro Yasue, Manabu Abe, Xulu Ye, Toshikuni Sasaoka, Masanori Tsuchida, Kenji Sakimura, Yoichi Ajioka, Yasuo Saijo, Qiliang Zhou

    CELL REPORTS   31 ( 6 )   107626 - 107626   2020.5

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    DOI: 10.1016/j.celrep.2020.107626

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  • Generation of Thyroid Tissues From Embryonic Stem Cells via Blastocyst Complementation In Vivo. Reviewed International journal

    Qingsong Ran, Qiliang Zhou, Kanako Oda, Akihiro Yasue, Manabu Abe, Xulu Ye, Yingchun Li, Toshikuni Sasaoka, Kenji Sakimura, Yoichi Ajioka, Yasuo Saijo

    Frontiers in endocrinology   11   609697 - 609697   2020

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    The generation of mature, functional, thyroid follicular cells from pluripotent stem cells would potentially provide a therapeutic benefit for patients with hypothyroidism, but in vitro differentiation remains difficult. We earlier reported the in vivo generation of lung organs via blastocyst complementation in fibroblast growth factor 10 (Fgf10), compound, heterozygous mutant (Fgf10 Ex1mut/Ex3mut) mice. Fgf10 also plays an essential role in thyroid development and branching morphogenesis, but any role thereof in thyroid organogenesis remains unclear. Here, we report that the thyroids of Fgf10 Ex1mut/Ex3mut mice exhibit severe hypoplasia, and we generate thyroid tissues from mouse embryonic stem cells (ESCs) in Fgf10 Ex1mut/Ex3mut mice via blastocyst complementation. The tissues were morphologically normal and physiologically functional. The thyroid follicular cells of Fgf10 Ex1mut/Ex3mut chimeric mice were derived largely from GFP-positive mouse ESCs although the recipient cells were mixed. Thyroid generation in vivo via blastocyst complementation will aid functional thyroid regeneration.

    DOI: 10.3389/fendo.2020.609697

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  • Nephrin-Binding Ephrin-B1 at the Slit Diaphragm Controls Podocyte Function through the JNK Pathway Reviewed International journal

    Yoshiyasu Fukusumi, Ying Zhang, Ryohei Yamagishi, Kanako Oda, Toru Watanabe, Katsuyuki Matsui, Hiroshi Kawachi

    JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY   29 ( 5 )   1462 - 1474   2018.5

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    DOI: 10.1681/ASN.2017090993

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  • Striatal hypodopamine phenotypes found in transgenic mice that overexpress glial cell line-derived neurotrophic factor Reviewed International journal

    Hidekazu Sotoyama, Yuriko Iwakura, Kanako Oda, Toshikuni Sasaoka, Nobuyuki Takei, Akiyoshi Kakita, Hideki Enomoto, Hiroyuki Nawa

    NEUROSCIENCE LETTERS   654   99 - 106   2017.7

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    DOI: 10.1016/j.neulet.2017.06.005

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  • Sirh7/Ldoc1 knockout mice exhibit placental P4 overproduction and delayed parturition Reviewed International journal

    Mie Naruse, Ryuichi Ono, Masahito Irie, Kenji Nakamura, Tamio Furuse, Toshiaki Hino, Kanako Oda, Misho Kashimura, Ikuko Yamada, Shigeharu Wakana, Minesuke Yokoyama, Fumitoshi Ishino, Tomoko Kaneko-Ishino

    DEVELOPMENT   141 ( 24 )   4763 - 4771   2014.12

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    DOI: 10.1242/dev.114520

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  • Pioneering Axons Regulate Neuronal Polarization in the Developing Cerebral Cortex Reviewed International journal

    Takashi Namba, Yuji Kibe, Yasuhiro Funahashi, Shinichi Nakamuta, Tetsuya Takano, Takuji Ueno, Akiko Shimada, Sachi Kozawa, Mayumi Okamoto, Yasushi Shimoda, Kanako Oda, Yoshino Wada, Tomoyuki Masuda, Akira Sakakibara, Michihiro Igarashi, Takaki Miyata, Catherine Faivre-Sarrailh, Kosei Takeuchi, Kozo Kaibuchi

    NEURON   81 ( 4 )   814 - 829   2014.2

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    DOI: 10.1016/j.neuron.2013.12.015

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  • Chondroitin sulphate N-acetylgalactosaminyl-transferase-1 inhibits recovery from neural injury Reviewed International journal

    Kosei Takeuchi, Nozomu Yoshioka, Susumu Higa Onaga, Yumi Watanabe, Shinji Miyata, Yoshino Wada, Chika Kudo, Masayasu Okada, Kentaro Ohko, Kanako Oda, Toshiya Sato, Minesuke Yokoyama, Natsuki Matsushita, Masaya Nakamura, Hideyuki Okano, Kenji Sakimura, Hitoshi Kawano, Hiroshi Kitagawa, Michihiro Igarashi

    NATURE COMMUNICATIONS   4   2740 - 2740   2013.11

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    DOI: 10.1038/ncomms3740

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  • TAG-1-assisted progenitor elongation streamlines nuclear migration to optimize subapical crowding Reviewed International journal

    Mayumi Okamoto, Takashi Namba, Tomoyasu Shinoda, Takefumi Kondo, Tadashi Watanabe, Yasuhiro Inoue, Kosei Takeuchi, Yukiko Enomoto, Kumiko Ota, Kanako Oda, Yoshino Wada, Ken Sagou, Kanako Saito, Akira Sakakibara, Ayano Kawaguchi, Kazunori Nakajima, Taiji Adachi, Toshihiko Fujimori, Masahiro Ueda, Shigeo Hayashi, Kozo Kaibuchi, Takaki Miyata

    NATURE NEUROSCIENCE   16 ( 11 )   1556 - 1566   2013.11

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    DOI: 10.1038/nn.3525

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  • Point Mutation in Syntaxin-1A Causes Abnormal Vesicle Recycling, Behaviors, and Short Term Plasticity Reviewed International journal

    Yumi Watanabe, Norikazu Katayama, Kosei Takeuchi, Tetsuya Togano, Rieko Itoh, Michiko Sato, Maya Yamazaki, Manabu Abe, Toshiya Sato, Kanako Oda, Minesuke Yokoyama, Keizo Takao, Masahiro Fukaya, Tsuyoshi Miyakawa, Masahiko Watanabe, Kenji Sakimura, Toshiya Manabe, Michihiro Igarashi

    JOURNAL OF BIOLOGICAL CHEMISTRY   288 ( 48 )   34906 - 34919   2013.11

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    DOI: 10.1074/jbc.M113.504050

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  • Accelerated modification of the zona pellucida is the primary cause of decreased fertilizability of oocytes in the 129 inbred mouse strain. Reviewed International journal

    Toshiaki Hino, Kanako Oda, Kenji Nakamura, Hiroyuki Tateno, Yutaka Toyoda, Minesuke Yokoyama

    Zygote (Cambridge, England)   19 ( 4 )   315 - 22   2011.11

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    DOI: 10.1017/S0967199410000481

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  • Low fertility in vivo resulting from female factors causes small litter size in 129 inbred mice. Reviewed

    Toshiaki Hino, Kanako Oda, Kenji Nakamura, Yutaka Toyoda, Minesuke Yokoyama

    Reproductive medicine and biology   8 ( 4 )   157 - 161   2009.12

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    Purpose: 129 inbred mice show poor reproductive ability, as evidenced by small litters; however, the exact cause of this is unknown. In the present in vivo study we examined fertility and subsequent post-implantation development in an attempt to clarify the cause of small litter size in 129 mice. Methods: 129 or C57BL/6J females that displayed vaginal plugs 1 day after mating with males of the same strain were examined for the presence of fertilized eggs. Reciprocal matings were also performed between 129 and C57BL/6J mice. Subsequent post-implantation development of fertilized eggs was examined by dissecting females 18-19 days after the vaginal plugs were found. Results: Mean numbers of recovered eggs were 7.9 and 8.0 in 129 and C57BL/6J mice, respectively. Half of the recovered eggs were unfertilized in 129 mice, whereas all were fertilized in C57BL/6J mice. Mean numbers of live fetuses 18-19 days after mating were significantly lower in 129 mice (4.7) than in C57BL/6J mice (7.3). In different types of pairings using both strains of mice, the fertility was significantly lower whenever 129 females were used. Conclusions: The small litter size in 129 mice is caused by low fertility resulting from female factors.

    DOI: 10.1007/s12522-009-0024-y

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  • Marked Improvement of Fertility of Cryopreserved C57BL/6J Mouse Sperm by Depletion of Ca2+ in Medium Reviewed

    Rika Suzuki-Migishima, Toshiaki Hino, Miho Takabe, Kanako Oda, Fujio Migishima, Yoshiharu Morimoto, Minesuke Yokoyama

    JOURNAL OF REPRODUCTION AND DEVELOPMENT   55 ( 4 )   386 - 392   2009.8

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    DOI: 10.1262/jrd.20163

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  • Paternal deletion of Meg1/Grb10 DMR causes maternalization of the Meg1/Grb10 cluster in mouse proximal Chromosome 11 leading to severe pre- and postnatal growth retardation Reviewed International journal

    Hirosuke Shiura, Kenji Nakamura, Takafusa Hikichi, Toshiaki Hino, Kanako Oda, Rika Suzuki-Migishima, Takashi Kohda, Tomoko Kaneko-Ishino, Fumitoshi Ishino

    HUMAN MOLECULAR GENETICS   18 ( 8 )   1424 - 1438   2009.4

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    DOI: 10.1093/hmg/ddp049

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MISC

  • 凍結胚を用いた2段階エレクトロポレーション法による効率的な遺伝子改変マウスの作製

    小田佳奈子, 佐々木綾音, 平澤克哉, 作間赳法, 桑原沙耶香, 笹岡俊邦, 福田七穂

    日本実験動物学会総会講演要旨集(Web)   72nd   2025

  • 新潟大学動物実験施設における地震等へのリスク対応

    作間赳法, 平澤克哉, 足立周子, 佐々木綾音, 桑原沙耶香, 中村古都, 小田佳奈子, 福田七穂, 笹岡俊邦

    日本実験動物学会総会講演要旨集(Web)   72nd   2025

  • CRISPR/Cas9法を用いたHnrnpabコンディショナルノックアウトマウスの作製及びその解析

    鈴木りん, 小田佳奈子, 笹岡俊邦, 福田七穂

    日本実験動物学会総会講演要旨集(Web)   71st   2024

  • 新潟大学動物実験施設におけるゼブラフィッシュの飼育管理と検疫方法について

    平澤克哉, 足立周子, 小田佳奈子, 福田七穂, 笹岡俊邦

    日本実験動物技術者協会総会講演要旨集   57th   2023

  • マウスをモデルとした培養液中オクタン酸の胚発生に与える影響

    田中宏明, 小田佳奈子, 山中紋奈, 小島淳哉, 小野政徳, 山田満稔, 浜谷敏生, 田中守, 笹岡俊邦, 西洋孝, 久慈直昭

    日本生殖医学会雑誌   68 ( 4 )   2023

  • 体外培養液中のオクタン酸ナトリウム濃度がマウス初期胚の発生に与える影響

    小田佳奈子, 笹岡俊邦, 久慈直昭

    日本実験動物学会総会講演要旨集(Web)   70th   2023

  • The impact of protein stabilizer octanoic acid in culture medium on murine embryo development

    山中紋奈, 土田奈々枝, 小島淳哉, 久慈直昭, 西洋孝, 山田満稔, 浜谷敏生, 小田佳奈子, 笹岡俊邦, 阿久津英憲

    東京医科大学雑誌(Web)   81 ( 2 )   2023

  • マウス胚操作に使用するミネラルオイルの検定

    阿部紗也香, 小田佳奈子, 福田七穂, 笹岡俊邦

    日本実験動物技術者協会総会講演要旨集   57th   2023

  • 夏季における外調機の給気温度変更による省エネルギー活動報告

    作間赳法, 小田佳奈子, 福田七穂, 笹岡俊邦

    日本実験動物技術者協会総会講演要旨集   56th (CD-ROM)   2022

  • 新潟大学動物実験施設における過去5年間の微生物モニタリング検査の結果報告

    平澤克哉, 作間赳法, 山本美丘, 小田佳奈子, 内山澄香, 齊藤奈英, 福田七穂, 笹岡俊邦

    日本実験動物技術者協会総会講演要旨集   56th (CD-ROM)   2022

  • 胚盤胞補完法を用いた効率的なキメラマウス作成条件の検討

    小田佳奈子, 阿部学, 夏目里恵, 崎村建司, 内山澄香, 齊藤奈英, 作間赳法, 西條康夫, 周啓亮, 笹岡俊邦

    日本実験動物学会総会講演要旨集(Web)   69th   2022

  • ポリA付加配列の挿入による長鎖3’UTRバリアントの生理機能の解明

    福田七穂, 小田佳奈子, 佐々木綾音, 齊藤奈英, 笹岡俊邦

    日本実験動物学会総会講演要旨集(Web)   69th   2022

  • 施設構造の特徴からみる衛生害虫チャタテムシの侵入経路とその対策

    作間赳法, 阿部光寿, 鈴木康浩, 小田佳奈子, 福田七穂, 笹岡俊邦

    日本実験動物技術者協会総会講演要旨集   55th   2021

  • Generation of lung organ from mouse embryonic stem cells in FGF10 gene knockout mice

    西條康夫, 周啓亮, 冉慶松, 北原哲彦, 小田佳奈子, 泰江章博, 笹岡俊邦, 叶許緑, 阿部学, 崎村建司, 土田正則, 味岡洋一

    日本呼吸器学会誌(Web)   10   2021

  • 胚盤胞補完法を利用したマウスES細胞による肺再生

    北原 哲彦, 周 啓亮, 冉 慶松, 叶 許緑, 小田 佳奈子, 笹岡 俊邦, 阿部 学, 崎村 建司, 味岡 洋一, 泰江 章博, 土田 正則, 西條 康夫

    日本外科学会定期学術集会抄録集   118回   1340 - 1340   2018.4

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  • D1/D2ドーパミン受容体コンディショナル発現マウスによる運動制御機構の解明

    笹岡 俊邦, 佐藤 朝子, 知見 聡美, 大久保 直, 阿部 学, 川村 名子, 中尾 聡宏, 齊藤 奈英, 酒井 清子, 小田 佳奈子, 前田 宜俊, 神保 幸弘, 田中 稔, 山本 美丘, 佐藤 俊哉, 藤澤 信義, 崎村 建司, 南部 篤

    生命科学系学会合同年次大会   2017年度   [4LT08 - 1195)]   2017.12

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  • EIF2B5<sup>toy</sup>:進行性の運動障害を示す突然変異マウスの発見と解析

    照光(辻田)実加, 北浦弘樹, 三浦郁生, 小田佳奈子, 清家尚彦, 豊島靖子, 若菜茂晴, 五十嵐博中, 中田力

    日本分子生物学会年会プログラム・要旨集(Web)   39th   2016

  • D1ドーパミン受容体を介するシグナルによる運動量の維持

    笹岡 俊邦, 佐藤 朝子, 知見 聡美, 大久保 直, 前島 純, 新井 慧, 砂山 智子[森田], 小田 佳奈子, 酒井 清子, 前田 宜俊, 神保 幸弘, 馬川 恵梨子, 佐藤 俊哉, 藤澤 信義, 横山 峯介, 南部 篤

    日本生化学会大会・日本分子生物学会年会合同大会講演要旨集   88回・38回   [3P1337] - [3P1337]   2015.12

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  • 【精神疾患動物モデルの可能性と課題】統合失調症モデルマウスの行動解析方法の試み

    笹岡 俊邦, 佐藤 朝子, 中村 徹, 大久保 直, 佐藤 俊哉, 藤澤 信義, 前田 宜俊, 小田 佳奈子, 酒井 清子, 神保 幸弘, 馬川 恵梨子, 木津川 尚史, 籾山 俊彦, 山森 哲雄

    日本生物学的精神医学会誌   26 ( 2 )   87 - 94   2015.6

  • ポドサイト機能維持におけるEphrin B1の役割 KOマウスを用いた解析

    福住 好恭, 小田 佳奈子, 河内 裕

    日本腎臓学会誌   57 ( 3 )   566 - 566   2015.4

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  • 初期胚の体外培養がマウスの個体発生に及ぼす影響

    小田 佳奈子

    新潟医学会雑誌   128 ( 12 )   635 - 646   2014.12

  • D1ドーパミン受容体の発現抑制によりマウスの自発運動量が低下する

    笹岡俊邦, 佐藤朝子, 新井慧, 前島純, 大久保直, 藤澤信義, 佐藤俊哉, 小田佳奈子, 前田宜俊, 田中稔, 山本美丘, 酒井清子, 神保幸弘, 千葉さおり, 横山峯介, 横山峯介

    日本実験動物学会総会講演要旨集   61st   2014

  • 人工制限酵素による内在性TDP-43遺伝子改変と筋萎縮性側索硬化症モデルへの応用

    佐藤 俊哉, 小田 佳奈子, 酒井 清子, 廣川 祥子, 永田 史也, 前田 宜俊, 藤澤 信義, 西澤 正豊, 小野寺 理, 横山 峯介

    臨床神経学   53 ( 12 )   1500 - 1500   2013.12

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    Language:Japanese   Publisher:(一社)日本神経学会  

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  • 日本哺乳動物卵子学会によるヒト胚培地の開発 マウス胚による検討

    横山 峯介, 小田 佳奈子

    Journal of Mammalian Ova Research   29 ( 2 )   S8 - S8   2012.4

  • 細胞内膜構造に注目した運動神経病の画期的な治療法の開発 TDP-43遺伝子改変マウスの作成と疾患モデルへの応用

    佐藤俊哉, 廣川祥子, 小田佳奈子, 横山峯介, 西澤正豊, 崎村建司, 小野寺理

    細胞内膜班構造に注目した運動神経病の画期的な治療法の開発班 平成23年度 総括・分担研究報告書   2012

  • 129系マウス卵子における受精障害の原因の解明

    日野 敏昭, 小田 佳奈子, 中村 健司, 立野 裕幸, 豊田 裕, 横山 峯介

    Journal of Mammalian Ova Research   27 ( 2 )   S61 - S61   2010.4

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  • Study of small litter size in 129 mice

    HINO Toshiaki, ODA Kanako, NAKAMURA Kenji, TOYODA Yutaka, YOKOYAMA Minesuke

    26 ( 2 )   S78   2009.4

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  • 129系マウスにおける低い体外受精率の検討

    日野 敏昭, 小田 佳奈子, 横山 峯介

    日本生殖医学会雑誌   53 ( 4 )   269 - 269   2008.10

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  • マウスMeg1/Grb10領域のインプリンティング発現制御と個体成長への影響

    志浦寛相, 引地貴亮, 中村健司, 日野敏昭, 小田佳奈子, 鈴木(右島)理可, 幸田尚, 金児(石野)知子, 石野史敏

    生化学   2008

  • ブタ顆粒膜細胞は種々の間葉系細胞に分化転換する

    小田 佳奈子, 加野 浩一郎

    日本発生生物学会大会講演要旨集   38回   240 - 240   2005.5

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  • ブタ顆粒膜細胞は種々の間葉系細胞に分化転換する

    小田 佳奈子, 遠藤 克, 加野 浩一郎

    日本畜産学会大会講演要旨集   104回   204 - 204   2005.3

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Research Projects

  • 嗅軸索で局所翻訳されるmRNAの網羅的特定と、局所翻訳の機構・意義の包括的な理解

    Grant number:25K02452

    2025.4 - 2028.3

    System name:科学研究費助成事業

    Research category:基盤研究(B)

    Awarding organization:日本学術振興会

    福田 七穂, 元岡 大祐, 小田 佳奈子, 福田 智行

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    Grant amount:\18720000 ( Direct Cost: \14400000 、 Indirect Cost:\4320000 )

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  • 気管移植を目指した胚盤胞補完法による生体内気管再生

    Grant number:24K11760

    2024.4 - 2027.3

    System name:科学研究費助成事業

    Research category:基盤研究(C)

    Awarding organization:日本学術振興会

    周 ケイリョウ, 笹岡 俊邦, 小田 佳奈子

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    Grant amount:\4550000 ( Direct Cost: \3500000 、 Indirect Cost:\1050000 )

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  • 胚盤胞補完法による臓器再生への応用に向けたナイーブ型脱分化脂肪細胞(DFAT)の樹立

    Grant number:24K11781

    2024.4 - 2027.3

    System name:科学研究費助成事業

    Research category:基盤研究(C)

    Awarding organization:日本学術振興会

    小田 佳奈子

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    Grant amount:\1820000 ( Direct Cost: \1400000 、 Indirect Cost:\420000 )

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  • 嗅神経軸索におけるmRNA局所翻訳の機構と生理的意義の解明

    Grant number:22K06895

    2022.4 - 2025.3

    System name:科学研究費助成事業

    Research category:基盤研究(C)

    Awarding organization:日本学術振興会

    福田 七穂, 小田 佳奈子

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    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

    神経細胞では、軸索や樹状突起などの細胞体から離れた部位において、特定のmRNAが局所的に翻訳されることが知られている。このような「mRNA局所翻訳」は、軸索伸長やシナプス可塑性を担い、神経疾患にも関連することから、その機構の解明が求められている。
    私達はこれまでに、RNA結合タンパク質 hnRNP A/Bの欠損マウスにおいて、嗅神経回路の形成不全が生じることを見出した。hnRNP A/Bの主要な標的遺伝子であるProtocadhelin alpha(Pcdha)は、hnRNP A/B依存的に嗅神経細胞の軸索末端に強く発現していた。このことから、hnRNP A/BがPcdhaの軸索末端における発現制御を介して嗅神経回路の形成を担う可能性が示唆された。そこで、令和5年度はPcdha遺伝子の3'-UTRからhnRNP A/B認識配列を含む領域を欠失させたマウス(Pcdha-UTR欠失マウス)を作製し、解析した。Pcdha-UTR欠失マウスでは、嗅神経細胞におけるhnRNP A/BとPcdha mRNAとの結合が低下した。また、嗅神経細胞の細胞体側におけるPCDHAタンパク質の発現に変化は見られないものの、軸索末端におけるPCDHAタンパク質の発現に有意な低下が見られた。さらに、重要なことに、Pcdha-UTR欠失マウスでは嗅神経回路の形成不全が認められた。これらの結果から、hnRNP A/Bは3'-UTR上の認識配列を介して神経回路形成に関わる因子のmRNAに結合し、それらの軸索末端におけるタンパク質発現を促進することにより、嗅神経回路の形成に寄与していることが示され、論文に発表した。

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  • Generation of purely pluripotent stem cell derived lung organ

    Grant number:21H02923

    2021.4 - 2024.3

    System name:Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

    Research category:Grant-in-Aid for Scientific Research (B)

    Awarding organization:Japan Society for the Promotion of Science

    SAIJO YASUO

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    Grant amount:\16250000 ( Direct Cost: \12500000 、 Indirect Cost:\3750000 )

    This study aims to ultimately create lungs derived 100% from embryonic stem cells. Mouse ES cells were cultured in three dimensions to attempt the creation of pseudo-embryos. ES cells cultured in ESLIF medium were started in a 96 well plate, and the culture was continued with a change to N2B27 medium containing Chiron, promoting the development and differentiation of gastruloids. As a result of trying various conditions, the ES cells aggregated and formed an individual entity. Histologically, the development of the primitive gut or lung buds was not confirmed. Also, genetic analysis did not confirm the expression of genes involved in lung development. In addition, research on lung regeneration by blastocyst complementation method was continued. By transplanting rat ES cells into mice with lung deficiencies, lung regeneration was successful in five cases. Further analysis confirmed the creation of lungs derived from rat ES cells

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  • Generation of lungs by blastocyst complementation in interspecific setting using ES cells

    Grant number:20H03741

    2020.4 - 2024.3

    System name:Grants-in-Aid for Scientific Research

    Research category:Grant-in-Aid for Scientific Research (B)

    Awarding organization:Japan Society for the Promotion of Science

    ZHOU Qiliang

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    Grant amount:\17420000 ( Direct Cost: \13400000 、 Indirect Cost:\4020000 )

    We succeeded in the generation of lungs using mouse embryonic stem cells(ESCs) in apneumic Fgf10 Ex1mut/Ex3mut mice by blastocyst complementation. Then, we show that rat ESCs can rescue the lung organization in mouse by interspecific blastocyst complementation. Lungs in the chimera mouse were efficiently derived from the venus positive rat ESCs.
    An interspecific blastocyst complementation method using chimeric animals may be useful as a way to create lung in animals.

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  • Effect of Octanoic acid and lipid metabolism in preembryo and pluripotent stem cells culture

    Grant number:15K10692

    2015.4 - 2018.3

    System name:Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    KUJI NAOAKI

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    Grant amount:\4810000 ( Direct Cost: \3700000 、 Indirect Cost:\1110000 )

    It was demonstrated that commercially available human in-vitro fertilization medium had contained 500uM-1000uM octanoic acid, using mass spectrometric analysis. Using F1 and inbred mice in-vitro fertilized embryo, several effects were recognized in the medium containing 800 and 1200uM of OA ; 1) in vitro embryo development (up to blastocyst stage) were delayed and disturbed, 2) implantation rates were decreased and 3) body weight were decreased after 179days after birth. Gene expression analysis revealed that expression pattern were different in several genes, including imprinting genes.

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  • Searching genes regulating VWM disease severity.

    Grant number:15K06909

    2015.4 - 2018.3

    System name:Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

    Tsujita Mika, ODA Kanako, KITAURA Hiroki

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    Grant amount:\5070000 ( Direct Cost: \3900000 、 Indirect Cost:\1170000 )

    Vanishing white matter (VWM) disease is known to have a wide range of severity of, but the pathological determinants at the molecular level have not been clarified. In this study, we tried Quantitative trait locus (QTL) analysis and influence factor search using gene expression analysis using causative gene mutant mouse of VWM disease. In the genetic background of B6 and C3H strains, the difference in the start timings of walking abnormalities in mutant mice was evident, and as a result of QTL analysis using this as an indicator, correlated chromosomal regions were detected. In this region, several genes showed marked differences in expression levels (e.g., ion transporter and apolipoprotein related genes). This method will be useful for elucidating the molecular level of the pathology of VWM disease.

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  • GENERATION OF LUNG ORGAN FROM EMBRYONIC STEM CELLS VIA BLASTOCYST COMPLEMENTATION IN MIC

    Grant number:15K15320

    2015.4 - 2017.3

    System name:Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research

    Research category:Grant-in-Aid for Challenging Exploratory Research

    Awarding organization:Japan Society for the Promotion of Science

    SAIJO YASUO, SAKIMURA KENJI, OHUCHI HIDEYO

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    Grant amount:\3510000 ( Direct Cost: \2700000 、 Indirect Cost:\810000 )

    We have developed Fgf10-/- mice by CRISPR/Cas system . Since the Fgf10-/- die immediately after birth, the Fgf10+/- genotype mice are maintained. We implanted 40 control embryos that was not injected ES cells into pseudopregnant mice and we obtained 13 littermates (32.5%) from the mice. 4 littermates (30.7%) showed limb defect (Fgf10-/-) and they were confirmed histologically that they had hypoplastic or aplastic lung. EGFPposotive ES cells were injected into blacystocyte of Fgf10-/- mice. 45 littermates were obtained from those mice. 38 littermates were EGFP positive. All EGFP positive mice showed the lung organ histologically. We sacrificed and analyzed histology in EGFP positive mice over one month. EGFP was positive in their lungs. The tissue, cells, and structure of their lung were well developed and not different from normal mice lung by H-E staining. Frozen section of the lung showed EGFP positive in alveolar epithelium, endothelium, tracheal cartilage.

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  • Technical development of transplantation human iPS induced hapatoblast and hepatocyte to mice embryos.

    Grant number:26640060

    2014.4 - 2018.3

    System name:Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Exploratory Research

    Research category:Grant-in-Aid for Challenging Exploratory Research

    Awarding organization:Japan Society for the Promotion of Science

    MORITA KUNIE

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    Grant amount:\3900000 ( Direct Cost: \3000000 、 Indirect Cost:\900000 )

    This research has conducrted 4 years, from fiscal year 2013 to 2017. The first year of this research, the research reader had changed the laboratory, from Kumamoto University to Niigata University of Health and Welfare. We were granted human iPS cells fron RIKEN, and we strarted differentiation- induced experiment from iPS cells to hepatocytes. And then, we confirmed differentiation to hepatocytes by means of immunological staining, hepatocyes marker ALB, SERPINA1 and HNF4A.
    This achivemnnt would help education and research for unversity students trying to be medical techcologysts, the reseach reader instructed there.

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  • Elucidation of motor control mechanism by D1 / D2 dopamine receptor conditionally expressing mice

    Grant number:26290029

    2014.4 - 2017.3

    System name:Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)

    Research category:Grant-in-Aid for Scientific Research (B)

    Awarding organization:Japan Society for the Promotion of Science

    SASAOKA Toshikuni, NAKAO Satohiro, NAMBU Atsushi, CHIKEN Satomi

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    Grant amount:\16900000 ( Direct Cost: \13000000 、 Indirect Cost:\3900000 )

    Using genetically modified mice that reversibly suppress expression of dopamine D1 receptor (D1R) by drug (doxycycline) administration, D1R deficiency leads to decrease of motor activity. Normally, the electrical stimulation at motor cortex travels through three pathways (hyper-direct, direct and indirect pathways) and is recorded as neural activity of triphasic "excitation - suppression - excitement" in the entopeduncular nucleus, the output part of the basal ganglia. In the state of D1R deficiency, 'suppression' disappeared. It is believed that this "suppression" passes through the direct pathway of the basal ganglia circuit and works for induction of movement. In this study, information via D1R is thought to be indispensable for signaling of the direct pathway and induction of movement, and a decrease in the dynamic transmission of signals through the direct pathway is thought to lead to motor symptoms of Parkinson's disease.

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Teaching Experience (researchmap)