Updated on 2024/07/28

Information

 

写真a

 
KYUMOTO YUKARI
 
Organization
Faculty of Dental Science Department of Dental Science Assistant Professor
School of Dentistry Department of Dentistry(Joint Appointment)
Graduate School of Dental Science (Joint Appointment)
Graduate School of Dental Science Department of Dental Science(Joint Appointment)
Title
Assistant Professor
Contact information
メールアドレス
Tel
0926426302
Profile
<研究活動> ・破骨細胞の細胞融合に関する研究 ・糖尿病関連因子と骨代謝 <教育活動> ・学部学生への解剖学実習補助 ・大学院生への研究指導
External link

Degree

  • PhD

Research Interests・Research Keywords

  • Research theme:Interaction between bone and adipose tissue and control of obesity and glucose metabolism through the secretion factors derived from osteoclasts

    Keyword:osteoclast, adipocyte, glucose metabolism

    Research period: 2016.4

  • Research theme:Effect of retinol binding protein 4 (RBP4) on bone destruction

    Keyword:osteoclast, bone destruction, diabetes

    Research period: 2014.9 - 2016.3

  • Research theme:Tim3/Galectin-9 system in the modulation of bone destruction

    Keyword:osteoclast, bone resorption

    Research period: 2014.2

  • Research theme:Comparison of osteoclasts and foreign body giant cells and search for molecules that are specific to only fusion of osteoclasts

    Keyword:osteoclast, bone resorption, FBGC, cell fusion

    Research period: 2014.2

Papers

  • Extremely High Expression of Antisense RNA for Wilms' Tumor 1 in Active Osteoclasts: Suppression of Wilms' Tumor 1 Protein Expression during Osteoclastogenesis. Reviewed International journal

    Li YJ., Kukita A., Kyumoto-Nakamura Y., Kukita T.

    186 ( 9 )   2317 - 25   2016.9

     More details

    Language:Japanese   Publishing type:Research paper (scientific journal)  

    Extremely High Expression of Antisense RNA for Wilms' Tumor 1 in Active Osteoclasts: Suppression of Wilms' Tumor 1 Protein Expression during Osteoclastogenesis.
    Wilms' tumor 1 (WT1), a zinc-finger transcription regulator of the early growth response family, identified as the product of a tumor suppressor gene of Wilms' tumors, bears potential ability to induce macrophage differentiation in blood cell differentiation. Herein, we examined the involvement of WT1 in the regulation of osteoclastogenesis. We detected a high level of WT1 protein expression in osteoclast precursors; however, WT1 expression was markedly suppressed during osteoclastogenesis. We examined expression of WT1 transcripts in bone tissue by RNA in situ hybridization. We found a high level of antisense transcripts in osteoclasts actively resorbing bone in mandible of newborn rats. Expression of antisense WT1 RNA in mandible was also confirmed by Northern blot analysis and strand-specific RT-PCR. Overexpression of antisense WT1 RNA in RAW-D cells, an osteoclast precursor cell line, resulted in a marked enhancement of osteoclastogenesis, suggesting that antisense WT1 RNA functions to suppress expression of WT1 protein in osteoclastogenesis. High level expression of antisense WT1 RNA may contribute to commitment to osteoclastogenesis, and may allow osteoclasts to maintain or stabilize their differentiation state.

    DOI: 10.1016/j.ajpath.2016.05.005

  • Growth differentiation factor-5 promotes brown adipogenesis in systemic energy expenditure. Reviewed International journal

    Hinoi E., Nakamura Y., Takada S., Fujita H., Iezaki T., Hashizume S., Takahashi S., Odaka Y., Watanabe T., Yoneda Y.

    Diabetes   63 ( 1 )   162 - 175   2014.1

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.2337/db13-0808

  • Repression of adipogenesis through promotion of Wnt/ß-catenin signaling by TIS7 up-regulated in adipocytes under hypoxia. Reviewed International journal

    1832 ( 8 )   1117 - 1128   2013.8

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    Although tetradecanoyl phorbol acetate induced sequence-7 (TIS7) has been identified as a co-activator/repressor of gene transcription in different eukaryotic cells, little attention has been paid to the functionality of TIS7 in adipocytes. Here, we evaluated the possible role of TIS7 in mechanisms underlying the regulation of adipogenesis. TIS7 expression was preferentially up-regulated in white adipose tissues (WAT) of obesity model mice as well as in pre-adipocytic 3T3-L1 cells cultured under hypoxic conditions. TIS7 promoter activity was selectively enhanced by activating transcription factor-6 (ATF6) among different transcription factors tested, while induction of TIS7 by hypoxic stress was markedly prevented by knockdown of ATF6 by shRNA in 3T3-L1 cells. Overexpression of TIS7 markedly inhibited Oil Red O staining and expression of particular adipogenic genes in 3T3-L1 cells. TIS7 synergistically promoted gene transactivation mediated by Wingless-type mouse mammary tumor virus integration site family (Wnt)/β-catenin, while blockade of the Wnt/β-catenin pathway by a dominant negative form of T-cell factor-4 (DN-TCF4) markedly prevented the inhibition of adipogenesis in 3T3-L1 cells with TIS7 overexpression. TIS7 predominantly interacted with β-catenin in the nucleus of WAT in the genetically obese ob/ob mice as well as in 3T3-L1 cells cultured under hypoxic conditions. Both knockdown of TIS7 by shRNA and introduction of DN-TCF4 similarly reversed the hypoxia-induced inhibition of adipogenic gene expression in 3T3-L1 cells. These findings suggest that TIS7 could play a pivotal role in adipogenesis through interacting with β-catenin to promote the canonical Wnt signaling in pre-adipocytes under hypoxic stress such as obesity.

    DOI: 10.1016/j.bbadis.2013.03.010

  • Osteoclastogenesis is negatively regulated by D-serine produced by osteoblasts. Reviewed International journal

    Takarada T., Takarada-Iemata M., Takahata Y., Yamada D., Yamamoto T., Nakamura Y., Hinoi E., Yoneda Y.

    J. Cell. Physiol.   227   3477 - 3487   2012.10

     More details

    Language:English  

  • Positive regulation by GABA(B) receptor subunit-1 of chondrogenesis through acceleration of nuclear translocation of activating transcription factor-4. Reviewed International journal

    Takahata Y., Hinoi E., Takarada T., Nakamura Y., Ogawa S., Yoneda Y.

    J. Biol. Chem.   287   33293 - 33303   2012.9

     More details

    Language:English  

  • Negative regulation of osteoblastogenesis through downregulation of runt-related transcription factor-2 in osteoblastic MC3T3-E1 cells with stable overexpression of the cystine/glutamate antiporter xCT subunit. Reviewed International journal

    Uno K., Takarada T., Takarada-Iemata M., Nakamura Y., Fujita H., Hinoi E., Yoneda Y.

    J. Cell. Physiol.   226   2953 - 2964   2011.11

     More details

    Language:English  

  • Osteoblastic GABAB receptors negatively regulate osteoblastogenesis toward disturbance of osteoclastogenesis mediated by receptor activator of nuclear factor-kB ligand in mouse bone. Reviewed International journal

    Takahata Y., Takarada T., Hinoi E., Nakamura Y., Fujita H., Yoneda Y.

    J. Biol. Chem.   286   32906 - 32917   2011.9

     More details

    Language:English  

  • Glutamate preferentially suppresses osteoblastogenesis than adipogenesis through the cystine/glutamate antiporter in mesenchymal stem cells. Reviewed International journal

    Takarada-Iemata M., Takarada T., Nakamura Y. Nakatani E., Hori O., Yoneda Y.

    J. Cell. Physiol.   226   652 - 665   2011.3

     More details

    Language:English  

  • Positive regulation by GABABR1 subunit of leptin expression through gene transactivation in adipocytes. Reviewed International journal

    Nakamura Y.*, Hinoi E.*, Takarada T., Takahata Y., Yamamoto T., Fujita H., Takada S., Hashizume S., Yoneda Y.

    PLoS ONE.   6   e20167   2011.3

     More details

    Language:English  

  • A negative correlation between expression profiles of runt-related transcription factor-2 and cystine/glutamate antiporter xCT subunit in ovariectomized mouse bone. Reviewed International journal

    Uno K., Takarada T., Nakamura Y., Fujita H., Hinoi E., Yoneda Y.

    J. Pharmacol. Sci.   115   309 - 319   2011.2

     More details

    Language:English  

  • Predominant promotion by tacrolimus of chondrogenic differentiation to proliferating chondrocytes. Reviewed International journal

    Nakamura Y.*, Takarada T.*, Kodama A., Hinoi E., Yoneda Y.

    J. Pharmacol. Sci.   109   413 - 423   2009.3

     More details

    Language:English  

  • Differential regulation of cellular maturation in chondrocytes and osteoblasts by glycine. Reviewed International journal

    Takahata Y., Takarada T., Osawa M., Hinoi E., Nakamura Y., Yoneda Y.

    Cell Tissue Res.   333   91 - 103   2008.7

     More details

    Language:English  

  • Erythropoietin receptor signal is crucial for periodontal ligament stem cell-based tissue reconstruction in periodontal disease. Reviewed International journal

    Mhd Fouad Zakaria, Soichiro Sonoda, Hiroki Kato, Lan Ma, Norihisa Uehara, Yukari Kyumoto-Nakamura, M Majd Sharifa, Liting Yu, Lisha Dai, Erika Yamauchi-Tomoda, Reona Aijima, Haruyoshi Yamaza, Fusanori Nishimura, Takayoshi Yamaza

    Scientific reports   14 ( 1 )   6719 - 6719   2024.3

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/s41598-024-57361-y

    Repository Public URL: https://hdl.handle.net/2324/7178660

  • miR-92a-3p encapsulated in bone metastatic mammary tumor cell–derived extracellular vesicles modulates mature osteoclast longevity Invited Reviewed International journal

    2022.12

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

  • In vitro and in vivo detection of tunneling nanotubes in normal and pathological osteoclastogenesis involving osteoclast fusion Reviewed International journal

    Jing-Qi Zhang, Akira Takahashi, Jiong-Yan Gu, Xiaoxu Zhang, Yukari Kyumoto-Nakamura, Akiko Kukita, Norihisa Uehara, Hidenobu Hiura, Takayoshi Yamaza, Toshio Kukita

    Laboratory Investigation   101 ( 12 )   1571 - 1584   2021.12

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/s41374-021-00656-9

  • Modulation of osteoclastogenesis through adrenomedullin receptors on osteoclast precursors: initiation of differentiation by asymmetric cell division Reviewed International journal

    Toshio Kukita, Hidenobu Hiura, Jiong-Yan Gu, Jing-Qi Zhang, Yukari Kyumoto-Nakamura, Norihisa Uehara, Sara Murata, Soichiro Sonoda, Takayoshi Yamaza, Ichiro Takahashi, Akiko Kukita

    Laboratory Investigation   101 ( 11 )   1449 - 1457   2021.11

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/s41374-021-00633-2

  • Targeting of Deciduous Tooth Pulp Stem Cell–Derived Extracellular Vesicles on Telomerase-Mediated Stem Cell Niche and Immune Regulation in Systemic Lupus Erythematosus Reviewed

    206 ( 12 )   3053 - 3063   2021.6

     More details

    Language:Others   Publishing type:Research paper (scientific journal)  

    Systemic transplantation of stem cells from human exfoliated deciduous teeth (SHED) is used to treat systemic lupus erythematosus (SLE)-like disorders in MRL/lpr mice. However, the mechanisms underlying the SHED-based therapy remain unclear. In this study, we hypothesized that trophic factors within SHED-releasing extracellular vesicles (SHED-EVs) ameliorate the SLE-like phenotypes in MRL/lpr mice. SHED-EVs were isolated from the culture supernatant of SHED. SHED-EVs were treated with or without RNase and systemically administered to MRL/lpr mice. Subsequently, recipient bone marrow mesenchymal stem cells (BMMSCs) isolated from SHED-EV-administered MRL/lpr mice were examined for the in vitro and in vivo activity of hematopoietic niche formation and immunoregulation. Furthermore, the recipient BMMSCs were secondarily transplanted into MRL/lpr mice. The systemic SHED-EV infusion ameliorated the SLE-like phenotypes in MRL/lpr mice and improved the functions of recipient BMMSCs by rescuing Tert mRNA-associated telomerase activity, hematopoietic niche formation, and immunoregulation. The secondary transplantation of recipient BMMSCs recovered the immune condition and renal functions of MRL/lpr mice. The RNase treatment depleted RNAs, such as microRNAs, within SHED-EVs, and the RNA-depleted SHED-EVs attenuated the benefits of SHED-EVs in MRL/lpr mice. Collectively, our findings suggest that SHED-secreted RNAs, such as microRNAs, play a crucial role in treating SLE by targeting the telomerase activity of recipient BMMSCs.

    DOI: 10.4049/jimmunol.2001312

  • Extracellular vesicles from deciduous pulp stem cells recover bone loss by regulating telomerase activity in an osteoporosis mouse model Reviewed International journal

    Soichiro Sonoda, Sara Murata, Kento Nishida, Hiroki Kato, Norihisa Uehara, Yukari N. Kyumoto, Haruyoshi Yamaza, Ichiro Takahashi, Toshio Kukita, Takayoshi Yamaza

    Stem Cell Research & Therapy   11 ( 1 )   296 - 296   2020.12

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1186/s13287-020-01818-0

  • 破骨細胞機能制御に関連する新規破骨細胞特異的膜表面抗原

    顧 炯炎, 久本 由香里, 寺町 順平, 日浦 秀暢, 張 旌旗, 張 暁旭, 上原 範久, 山座 孝義, 久木田 明子, 久木田 敏夫

    2020   205 - 205   2020.9

     More details

    Language:Japanese  

  • Characteristics of differentiation of osteoclast cells irradiated with active species in atmospheric oxygen plasma Reviewed

    Nobuya Hayashi, Yuki Inoue, Yukari Kyumoto, Toshio Kukita

    JAPANESE JOURNAL OF APPLIED PHYSICS   59   2020.6

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.35848/1347-4065/ab7ba9

  • Acetylsalicylic Acid Treatment and Suppressive Regulation of AKT Accelerate Odontogenic Differentiation of Stem Cells from the Apical Papilla Reviewed

    Yosuke Tanaka, Soichiro Sonoda, Haruyoshi Yamaza, Sara Murata, Kento Nishida, Yukari Kyumoto-Nakamura, Norihisa Uehara, Kazuaki Nonaka, Toshio Kukita, Takayoshi Yamaza

    Journal of Endodontics   45 ( 5 )   591 - 598.e6   2019.5

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.joen.2019.01.016

  • Osteoblast lineage-specific cell-surface antigen (A7) regulates osteoclast recruitment and calcification during bone remodeling Reviewed

    Tamer Badawy, Yukari Kyumoto-Nakamura, Norihisa Uehara, Jingqi Zhang, Soichiro Sonoda, Hidenobu Hiura, Takayoshi Yamaza, Akiko Kukita, Toshio Kukita

    Laboratory Investigation   99 ( 6 )   866 - 884   2019.1

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/s41374-018-0179-4

  • Suppression of AKT-mTOR signal pathway enhances osteogenic/dentinogenic capacity of stem cells from apical papilla Reviewed

    Yosuke Tanaka, Soichiro Sonoda, Haruyoshi Yamaza, Sara Murata, Kento Nishida, Shion Hama, Yukari Kyumoto-Nakamura, Norihisa Uehara, Kazuaki Nonaka, Toshio Kukita, Takayoshi Yamaza

    Stem Cell Research and Therapy   9 ( 1 )   2018.11

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1186/s13287-018-1077-9

  • Unique Osteoblast-Specific Cell-Surface Antigen Useful for Odondoblast Ontology and Dentin Regeneration Invited Reviewed International journal

    Tamer Badawy, Yukari Kyumoto-Nakamura, Norihisa Uehara, Jingqi Zhang, Hidenobu Hiura, Soichiro Sonoda, Takayoshi Yamaza, Akiko Kukita, Toshio Kukita

    International Journal of Oral Health & Dental Management   2 ( 2 )   1 - 7   2018.6

     More details

    Language:Japanese   Publishing type:Research paper (scientific journal)  

    Unique Osteoblast-Specific Cell-Surface Antigen Useful for Odontoblast Ontology and Dentin Regeneration

    DOI: 10.33425/2639-9490.1018

  • Exogenous nitric oxide stimulates the odontogenic differentiation of rat dental pulp stem cells Invited Reviewed International journal

    Sonoda S., Mei Y. F., Atsuta I., Danjo A., Yamaza H., Hama S., Nishida K., Tang R., Kyumoto-Nakamura Y., Uehara N., Kukita T., Nishimura F., Yamaza T.

    SCIENTIFIC REPORTS   8 ( 1 )   2018.2

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/s41598-018-21183-6

  • IL-1β Induces Pathologically Activated Osteoclasts Bearing Extremely High Levels of Resorbing Activity: A Possible Pathological Subpopulation of Osteoclasts, Accompanied by Suppressed Expression of Kindlin-3 and Talin-1 Invited Reviewed International journal

    200 ( 1 )   218 - 228   2018.1

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.4049/jimmunol.1602035

  • Osteoblast-derived Laminin-332 is a novel negative regulator of osteoclastogenesis in bone microenvironments Invited Reviewed International journal

    Uehara N., Kukita A., Kyumoto-Nakamura Y., Yamaza T., Yasuda H., Kukita T.

    LABORATORY INVESTIGATION   97 ( 10 )   1235 - 1244   2017.10

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/labinvest.2017.55

    Repository Public URL: https://hdl.handle.net/2324/7173558

  • The transcriptional modulator Ifrd1 controls PGC-1α expression under short-term adrenergic stimulation in brown adipocytes. Reviewed International journal

    284 ( 5 )   784 - 795   2017.3

     More details

    Language:Japanese   Publishing type:Research paper (scientific journal)  

    DOI: 10.1111/febs.14019

  • Transcriptional Modulator Ifrd1 Regulates Osteoclast Differentiation through Enhancing the NF-κB/NFATc1 Pathway. International journal

    36 ( 19 )   2451 - 63   2016.10

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    Bone homeostasis is maintained by the synergistic actions of bone-resorbing osteoclasts and bone-forming osteoblasts. Here, we show that the transcriptional coactivator/repressor interferon-related developmental regulator 1 (Ifrd1) is expressed in osteoclast lineages and represents a component of the machinery that regulates bone homeostasis. Ifrd1 expression was transcriptionally regulated in preosteoclasts by receptor activator of nuclear factor κB (NF-κB) ligand (RANKL) through activator protein 1. Global deletion of murine Ifrd1 increased bone formation and decreased bone resorption, leading to a higher bone mass. Deletion of Ifrd1 in osteoclast precursors prevented RANKL-induced bone loss, although no bone loss was observed under normal physiological conditions. RANKL-dependent osteoclastogenesis was impaired in vitro in Ifrd1-deleted bone marrow macrophages (BMMs). Ifrd1 deficiency increased the acetylation of p65 at residues K122 and K123 via the inhibition of histone deacetylase-dependent deacetylation in BMMs. This repressed the NF-κB-dependent transcription of nuclear factor of activated T cells, cytoplasmic 1 (NFATc1), an essential regulator of osteoclastogenesis. These findings suggest that an Ifrd1/NF-κB/NFATc1 axis plays a pivotal role in bone remodeling in vivo and represents a therapeutic target for bone diseases.

    DOI: 10.1128/MCB.01075-15

    Repository Public URL: https://hdl.handle.net/2324/7178661

  • Transcriptional Modulator Ifrd1 Regulates Osteoclast Differentiation through Enhancing the NF-κB/NFATc1 Pathway. Reviewed International journal

    2016.9

     More details

    Language:Japanese  

  • The Transcriptional Modulator Interferon-Related Developmental Regulator 1 in Osteoblasts Suppresses Bone Formation and Promotes Bone Resorption. Reviewed International journal

    Iezaki T., Onishi Y., Ozaki K., Fukasawa K., Takahata Y., Nakamura Y., Fujikawa K., Takarada T., Yoneda Y., Yamashita Y., Shioi G., Hinoi E.

    31 ( 3 )   573 - 584   2016.3

     More details

    Language:Japanese   Publishing type:Research paper (scientific journal)  

    The Transcriptional Modulator Interferon-Related Developmental Regulator 1 in Osteoblasts Suppresses Bone Formation and Promotes Bone Resorption.
    Bone homeostasis is maintained by the synergistic actions of bone-resorbing osteoclasts and bone-forming osteoblasts. Although interferon-related developmental regulator 1 (Ifrd1) has been identified as a transcriptional coactivator/repressor in various cells, little attention has been paid to its role in osteoblastogenesis and bone homeostasis thus far. Here, we show that Ifrd1 is a critical mediator of both the cell-autonomous regulation of osteoblastogenesis and osteoblast-dependent regulation of osteoclastogenesis. Osteoblast-specific deletion of murine Ifrd1 increased bone formation and decreased bone resorption, causing high bone mass. Ifrd1 deficiency enhanced osteoblast differentiation and maturation along with increased expression of Runx2 and osterix (Osx). Mechanistically, Ifrd1 deficiency increased the acetylation status of p65, a component of NF-κB, at residues K122 and K123 via the attenuation of the interaction between p65 and histone deacetylase (HDAC). This led to the nuclear export of p65 and a decrease in NF-κB-dependent Smad7 expression and the subsequent enhancement of Smad1/Smad5/Smad8-dependent transcription. Moreover, a high bone mass phenotype in the osteoblast-specific deletion of Ifrd1 was markedly rescued by the introduction of one Osx-floxed allele but not of Runx2-floxed allele. Coculture experiments revealed that Ifrd1-deficient osteoblasts have a higher osteoprotegerin (OPG) expression and a lower ability to support osteoclastogenesis. Ifrd1 deficiency attenuated the interaction between β-catenin and HDAC, subsequently increasing the acetylation of β-catenin at K49, leading to its nuclear accumulation and the activation of the β-catenin-dependent transcription of OPG. Collectively, the expression of Ifrd1 in osteoblasts repressed osteoblastogenesis and activated osteoclastogenesis through modulating the NF-κB/Smad/Osx and β-catenin/OPG pathways, respectively. These findings suggest that Ifrd1 has a pivotal role in bone homeostasis through its expression in osteoblasts in vivo and represents a therapeutic target for bone diseases.

    DOI: 10.1002/jbmr.2720

▼display all

Presentations

  • Galectin-9による破骨細胞分化制御メカニズムの解明:NFATc1の発現を抑制する転写因子MafB及びIRF-8の関与

    久本 由香里, 上原 範久, 久木田 明子, 久木田 敏夫

    第33回日本骨代謝学会学術集会  2015.7 

     More details

    Event date: 2015.7

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:新宿   Country:Japan  

  • 転写制御因子Ifrd1による脂肪細胞分化の調節

    中村 由香里, 檜井 栄一, 米田幸雄

    日本薬学会北陸支部第125回例会 

     More details

    Event date: 2013.11

    Language:Others   Presentation type:Oral presentation (general)  

    Venue:金沢   Country:Other  

  • 転写制御因子Ifrd1による脂肪細胞分化抑制機構

    中村 由香里, 檜井 栄一, 米田幸雄

    第122回日本薬理学会近畿部会 

     More details

    Event date: 2012.11

    Language:Others   Presentation type:Oral presentation (general)  

    Venue:大阪   Country:Other  

  • Ifrd1による脂肪細胞分化制御機構

    中村 由香里, 檜井 栄一, 米田幸雄

    次世代を担う創薬・医療薬理シンポジウム2012 

     More details

    Event date: 2012.9

    Language:Others   Presentation type:Oral presentation (general)  

    Venue:神戸   Country:Other  

  • 脂肪細胞分化調節機構における転写制御因子Ifrd1の役割

    中村 由香里, 檜井 栄一, 米田幸雄

    生体機能と創薬シンポジウム2012 

     More details

    Event date: 2012.8

    Language:Others   Presentation type:Symposium, workshop panel (public)  

    Venue:神戸   Country:Other  

  • 脂肪細胞における転写因子Ifrd1の機能

    中村 由香里, 檜井 栄一, 米田幸雄

    第121回日本薬理学会近畿部会 

     More details

    Event date: 2012.6

    Language:Others   Presentation type:Oral presentation (general)  

    Venue:徳島   Country:Other  

  • GABABR1サブユニットによる脂肪細胞のleptin発現調節

    中村 由香里, 檜井 栄一, 宝田 剛志, 高畑 佳史, 米田 幸雄

    日本薬学会北陸支部第123回例会 

     More details

    Event date: 2011.11

    Language:Others   Presentation type:Oral presentation (general)  

    Venue:金沢   Country:Other  

  • Positive regulation by GABABR1 subunit of leptin expression through gene transactivation in adipocytes

     More details

    Event date: 2011.5

    Language:Others   Presentation type:Symposium, workshop panel (public)  

    Country:Other  

  • 転写因子Ifrd1の脂肪細胞における発現

    中村 由香里, 檜井 栄一, 高田 紗矢, 宝田 剛志, 米田 幸雄

    第118回日本薬理学会近畿部会 

     More details

    Event date: 2010.11

    Language:Others   Presentation type:Oral presentation (general)  

    Venue:大阪   Country:Other  

  • GABABR1サブユニットによる脂肪細胞のleptin発現制御

    中村 由香里, 宝田 剛志, 檜井 栄一, 米田 幸雄

    第117回日本薬理学会近畿部会 

     More details

    Event date: 2010.7

    Language:Others   Presentation type:Oral presentation (general)  

    Venue:徳島   Country:Other  

  • 脂肪細胞分化におけるGABABレセプターの調節機能

    中村 由香里, 宝田 剛志, 檜井 栄一, 米田 幸雄

    日本薬学会第130年会 

     More details

    Event date: 2010.3

    Language:Others   Presentation type:Symposium, workshop panel (public)  

    Venue:岡山   Country:Other  

  • GABABR1サブユニット欠損マウスにおける脂肪分化調節

    中村 由香里, 宝田 剛志, 檜井 栄一, 米田 幸雄

    第83回日本薬理学会年会 

     More details

    Event date: 2010.3

    Language:Others   Presentation type:Symposium, workshop panel (public)  

    Venue:大阪   Country:Other  

  • 脂肪細胞におけるGABABR1サブユニットの機能

    中村 由香里, 宝田 剛志, 檜井 栄一, 米田 幸雄

    第116回日本薬理学会近畿部会 

     More details

    Event date: 2009.11

    Language:Others   Presentation type:Oral presentation (general)  

    Venue:滋賀   Country:Other  

  • Down-regulation of glutamate transporter expression by lipopolysaccharide in cultured astrocytes. International conference

    Nakamura, Y., Ogura, M., Taniura, H., Nakamichi, N. and Yoneda, Y.

    The 22nd Biennial Meeting of the ISN/APSN Joint Meeting 

     More details

    Event date: 2009.8

    Language:Others   Presentation type:Symposium, workshop panel (public)  

    Country:Korea, Republic of  

  • FK506による増殖期軟骨細胞分化の促進

    中村 由香里, 宝田 剛志, 米田 幸雄

    第27回日本骨代謝学会学術集会 

     More details

    Event date: 2009.7

    Language:Others   Presentation type:Symposium, workshop panel (public)  

    Venue:大阪   Country:Other  

  • 脂肪細胞に発現するGABAシグナル分子

    中村 由香里, 宝田 剛志, 米田 幸雄

    日本薬学会第129年会 

     More details

    Event date: 2009.3

    Language:Others   Presentation type:Symposium, workshop panel (public)  

    Venue:京都   Country:Other  

  • 根尖歯乳頭組織由来幹細胞に発現する転写因子PITX2の機能解析

    久本 由香里、園田 聡一朗、加藤 大樹、上原 範久、山座 孝義

    2023.9 

     More details

    Event date: 2023.9

    Language:Japanese  

    Venue:東京   Country:Japan  

  • Galectin-9/Tim-3シグナルを介した破骨細胞分化制御メカニズムの解明

    久本 由香里, 上原 範久, 久木田 明子, 山座 孝義, 久木田 敏夫

    第42回日本分子生物学会年会  2019.12 

     More details

    Event date: 2019.12

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Venue:福岡   Country:Japan  

  • 破骨細胞分化制御におけるGalectin-9/Tim-3シグナルの関与

    久本 由香里, 上原 範久, 久木田 明子, 久木田 敏夫

    第36回 日本骨代謝学会学術集会  2018.7 

     More details

    Event date: 2018.7

    Language:Japanese  

    Venue:長崎   Country:Japan  

  • Galectin-9による破骨細胞分化抑制因子MafBの発現制御

    久本 由香里, 上原 範久, 久木田 明子, 山座 孝義, 久木田 敏夫

    第58回 歯科基礎医学会  2016.8 

     More details

    Event date: 2016.8

    Language:Japanese  

    Venue:札幌   Country:Japan  

  • Galectin-9による破骨細胞分化抑制と転写因子MafBの発現制御メカニズムの解明

    久本 由香里, 上原 範久, 久木田 明子, 久木田 敏夫

    第34回 日本骨代謝学会学術集会  2016.7 

     More details

    Event date: 2016.7

    Language:Japanese  

    Venue:大阪   Country:Japan  

  • Galectin-9による破骨細胞形成抑制機構:MafB制御系関与の可能性

    久本 由香里, 上原 範久, 久木田 明子, 久木田 敏夫

    第57回歯科基礎医学会学術大会  2015.9 

     More details

    Event date: 2015.9 - 2016.9

    Language:Japanese  

    Venue:新潟   Country:Japan  

  • ラミニン-332によるRANK発現調節とマクロファージ-破骨細胞分化転換の制御

    久本 由香里, 上原 範久, 久木田 明子, 保田 尚孝, 久木田 敏夫

    第33回日本骨代謝学会学術集会  2015.7 

     More details

    Event date: 2015.7

    Language:Japanese   Presentation type:Symposium, workshop panel (public)  

    Country:Japan  

  • 細胞外マトリックス分子ラミニン332の破骨細胞形成抑制作用

    久本 由香里, 上原 範久, 久木田 明子, 保田 尚孝, 久木田 敏夫

    第14回 西日本骨・関節関連疾患懇話会  2015.7 

     More details

    Event date: 2015.7

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:九州大学   Country:Japan  

  • 免疫制御膜表面分子Tim-3を介する炎症性骨破壊制御

    森山 加奈子, 久木田 明子, 上原 範久, 久本 由香里, 髙橋 一郎, 久木田 敏夫

    第32回日本骨代謝学会学術集会  2014.7 

     More details

    Event date: 2014.7

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:大阪   Country:Japan  

  • 免疫調節膜表面分子Tim-3を介した炎症性骨破壊の効果的制御

    森山 加奈子, 久木田 明子, 上原 範久, 張 旌旗, 久本 由香里, 髙橋 一郎, 久木田 敏夫

    第13回西日本骨・関節関連疾患懇話会  2014.7 

     More details

    Event date: 2014.7

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:九州大学   Country:Japan  

  • GABABR1サブユニット分子による破骨細胞分化の調節

    高畑 佳史, 宝田 剛志, 中村 由香里, 檜井 栄一, 米田 幸雄

    第119回日本薬理学会近畿部会 

     More details

    Event date: 2011.7

    Language:Others   Presentation type:Oral presentation (general)  

    Venue:名古屋   Country:Other  

  • GABABR1サブユニット安定発現骨芽細胞株の機能解析

    高畑 佳史, 宝田 剛志, 中村 由香里, 米田 幸雄

    第27回日本骨代謝学会学術集会 

     More details

    Event date: 2009.7

    Language:Others   Presentation type:Symposium, workshop panel (public)  

    Venue:大阪   Country:Other  

  • 免疫調節分子Tim-3の破骨細胞での発現と炎症性骨破壊制御

    森山 加奈子, 久木田 明子, 上原 範久, 久本 由香里, 髙橋 一郎, 久木田 敏夫

    第56回歯科基礎医学会 

     More details

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡   Country:Japan  

  • Osteoclasts Formed under Stimulation by IL-1β Possess Extremely High Ability to Secrete Protons and to Resorb Dentin with Abnormal Adhesiveness, Imaged by pH-Sensitive Fluorescence Probes International conference

    2017.9 

     More details

    Language:English  

    Country:United States  

▼display all

Industrial property rights

Patent   Number of applications: 1   Number of registrations: 1
Utility model   Number of applications: 0   Number of registrations: 0
Design   Number of applications: 0   Number of registrations: 0
Trademark   Number of applications: 0   Number of registrations: 0

Professional Memberships

  • The Japanese Society for Bone and Mineral Research

  • Japanese Association for Oral Biiology

  • The Japanese Association of Anatomists

Research Projects

  • 病的活性化破骨細胞の骨吸収能亢進メカニズムの解明

    2022

    出産・育児復帰者支援

      More details

    Authorship:Principal investigator  Grant type:On-campus funds, funds, etc.

  • 糖尿病誘発因子を標的とした新規骨破壊制御法の開発に関する研究

    Grant number:21K16933  2021 - 2023

    日本学術振興会  科学研究費助成事業  若手研究

      More details

    Authorship:Principal investigator  Grant type:Scientific research funding

  • 病的活性化破骨細胞に発現する膜表面分子を標的とした病的骨破壊特異的制御法の開発

    Grant number:19K24098  2019 - 2020

    日本学術振興会  科学研究費助成事業  研究活動スタート支援

      More details

    Authorship:Principal investigator  Grant type:Scientific research funding

  • 破骨細胞由来生理活性物質を介した骨-脂肪コミュニケーションと肥満・糖代謝制御

    Grant number:16K20413  2016 - 2017

    科学研究費助成事業  若手研究(B)

      More details

    Authorship:Principal investigator  Grant type:Scientific research funding

  • 糖尿病誘発因子RBP4による骨破壊制御

    Grant number:26893194  2014 - 2015

    科学研究費助成事業  若手研究(スタートアップ)

      More details

    Authorship:Principal investigator  Grant type:Scientific research funding

  • 転写調節因子Ifrd1を標的とする生活習慣病の新規薬物治療法開発

    Grant number:24 2846  2012 - 2013

    日本学術振興会  科学研究費助成事業  特別研究員奨励費

      More details

    Authorship:Principal investigator  Grant type:Scientific research funding

▼display all

Class subject

  • 解剖学実習2

    2024.12 - 2025.2   Winter quarter

  • 解剖学実習1

    2024.10 - 2024.12   Fall quarter

  • 解剖学2

    2024.6 - 2024.8   Summer quarter

  • 解剖学1

    2024.4 - 2024.6   Spring quarter

  • 解剖学実習2

    2023.12 - 2024.2   Winter quarter

  • 解剖学実習1

    2023.10 - 2023.12   Fall quarter

  • 解剖学2

    2023.6 - 2023.8   Summer quarter

  • 解剖学1

    2023.4 - 2023.6   Spring quarter

  • 発生学

    2023.4 - 2023.6   Spring quarter

  • 解剖学実習2

    2022.12 - 2023.2   Winter quarter

  • 解剖学実習1

    2022.10 - 2022.12   Fall quarter

  • 口腔組織学1

    2022.6 - 2022.8   Summer quarter

  • 解剖学2

    2022.6 - 2022.8   Summer quarter

  • 口腔解剖学

    2022.4 - 2022.9   First semester

  • 発生学

    2022.4 - 2022.6   Spring quarter

  • 解剖学1

    2022.4 - 2022.6   Spring quarter

  • 口腔組織学Ⅱ

    2021.10 - 2022.3   Second semester

  • 解剖学

    2021.4 - 2022.3   Full year

  • 解剖学

    2020.4 - 2021.3   Full year

  • 硬組織研究法

    2020.4 - 2021.3   Full year

  • 発生学

    2020.4 - 2020.9   First semester

  • 分子口腔解剖学

    2019.4 - 2020.3   Full year

  • 解剖学

    2019.4 - 2020.3   Full year

  • 硬組織研究法

    2019.4 - 2020.3   Full year

  • 発生学

    2019.4 - 2019.9   First semester

  • 分子口腔解剖学

    2018.4 - 2019.3   Full year

  • 解剖学

    2018.4 - 2019.3   Full year

  • 硬組織研究法

    2018.4 - 2019.3   Full year

  • 発生学

    2018.4 - 2018.9   First semester

  • 解剖学

    2017.4 - 2018.3   Full year

  • 分子口腔解剖学

    2017.4 - 2018.3   Full year

  • 硬組織研究法

    2017.4 - 2018.3   Full year

  • 発生学

    2017.4 - 2017.9   First semester

  • 解剖学

    2016.4 - 2017.3   Full year

  • 硬組織研究法

    2016.4 - 2017.3   Full year

  • 分子口腔解剖学

    2016.4 - 2017.3   Full year

  • 発生学

    2016.4 - 2016.9   First semester

  • 解剖学

    2015.4 - 2016.3   Full year

  • 分子口腔解剖学

    2015.4 - 2016.3   Full year

  • 硬組織研究法

    2015.4 - 2016.3   Full year

  • 基幹教育セミナー

    2015.4 - 2015.9   First semester

  • 分子口腔解剖学演習

    2014.4 - 2015.3   Full year

  • 解剖学

    2014.4 - 2015.3   Full year

  • 分子口腔解剖学

    2014.4 - 2015.3   Full year

  • 硬組織研究法

    2014.4 - 2014.9   First semester

  • 口腔組織学Ⅱ

    2014.4 - 2014.9   First semester

  • 口腔細胞生物学

    2014.4 - 2014.9   First semester

▼display all

FD Participation

  • 2019.9   Role:Participation   Title:科研費申請のススメ!〜科学研究費補助金制度と研究計画調書作成時の注意点〜

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2017.10   Role:Participation   Title:第2回4部局合同男女共同参画FD

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2015.9   Role:Participation   Title:科学研究費改革の方向性、歯学教育の現状と課題

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2015.3   Role:Participation   Title:基幹教育セミナーのためのFD研修会

    Organizer:University-wide

  • 2014.9   Role:Participation   Title:科研費獲得のポイント

    Organizer:[Undergraduate school/graduate school/graduate faculty]

  • 2014.8   Role:Participation   Title:新GPA制度実施のためのFD

    Organizer:University-wide

  • 2014.4   Role:Participation   Title:第1回全学FD

    Organizer:University-wide

▼display all

Media Coverage

  • 「やせる脂肪」ともいわれる褐色脂肪細胞の分化を促進するある特定のサイトカインを確認した。 このサイトカインは、メタボリック症候群対策など、肥満を予防する新たな医薬品の開発などに活用が期待される。 Newspaper, magazine

    北國新聞  2011.6

     More details

    「やせる脂肪」ともいわれる褐色脂肪細胞の分化を促進するある特定のサイトカインを確認した。
    このサイトカインは、メタボリック症候群対策など、肥満を予防する新たな医薬品の開発などに活用が期待される。