Updated on 2022/05/12

写真a

 
OGAWA, Yasushi
 
Organization
Nagoya University Hospital Lecturer
Graduate School
Graduate School of Medicine
Title
Lecturer

Degree 1

  1. 博士(医学) ( 2004.11   名古屋大学 ) 

Research Interests 4

  1. chemical biology

  2. epigenetics

  3. inflammatory keratosis

  4. dermatology

Research Areas 2

  1. Others / Others  / Dermatology

  2. Life Science / Dermatology

Current Research Project and SDGs 2

  1. ケミカルバイオロジー的手法による皮膚疾患の解析

  2. 皮膚疾患におけるDFS70/LEDGFの役割

Research History 5

  1. Nagoya University   Department of Advanced Medicine, Nagoya University Hospital   Lecturer

    2020.5

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    Country:Japan

  2. Japan Agency for Medical Research and Development   Department of Research Promotion, Division of Rare / Intractable Disease Research   Deputy Manager

    2018.4 - 2020.4

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    Country:Japan

  3. Laboratory of Gene Expression, Graduate School of Biomedical Science, Tokyo Medical and Dental UniversityResearch Assistant Professor

    2007.1 - 2010.3

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    Country:Japan

  4. University of Texas Southwestern Medical Center at DallasDepartment of PathologyPostdoctoral fellow

    2005.4 - 2007.1

  5. University of Texas Southwestern Medical Center at DallasDepartment of DermatologyPostdoctoral Fellow

    2004.4 - 2005.3

Education 3

  1. Nagoya University   Graduate School of Medicine   Dermatology

    2000.4 - 2004.3

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    Country: Japan

  2. Nagoya University   Faculty of Medicine

    - 1998.3

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    Country: Japan

  3. Nagoya University   School of Medicine

    1992.4 - 1998.3

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    Country: Japan

Professional Memberships 4

  1. 加齢皮膚医学研究会

  2. The Japanese Pharmacological Society

  3. Japanese Dermatological Association

  4. The Japanese Society for Investigative Dermatology

Committee Memberships 1

  1. 日本皮膚科学会   医療戦略委員  

    2018.6   

Awards 3

  1. 第1回 高木賞

    2017   公益財団法人マルホ・高木皮膚科学振興財団  

  2. 第16回ガルデルマ賞

    2015  

  3. 加齢皮膚医学研究基金(ロート賞)

    2011   加齢皮膚医学研究会  

 

Papers 81

  1. Research impact analysis of international funding agencies in the realm of allergy and immunology Reviewed

    Takeya Adachi, Yasushi Ogawa, Tamami Fukushi, Kei Ito, Amane Koizumi, Masashi Shirabe, Masako Toriya, Jun Hirako, Takenori Inomata, Katsunori Masaki, Ryohei Sasano, Sakura Sato, Keigo Kainuma, Masaki Futamura, Keiko Kan-O , Yosuke Kurashima, Saeko Nakajima, Masafumi Sakashita, Hideaki Morita, Aikichi Iwamoto, Sankei Nishima, Mayumi Tamari, Hajime Iizuka

    Allergy     2022.5

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    Authorship:Lead author   Language:English  

    DOI: 10.1111/all.15249

  2. Evaluation of adrenaline auto-injector prescription profiles: A population-based, retrospective cohort study within the National Insurance Claims Database of Japan Reviewed

    Sakura Sato, Keigo Kainuma, Tatsuya Noda, Motohiro Ebisawa, Masaki Futamura, Tomoaki Imamura, Akihiro Miyagawa, Saeko Nakajima, Yasushi Ogawa, Takenori Inomata, Keiko Kan-O, Yosuke Kurashima, Katsunori Masaki, Tomoya Myojin, Yuichi Nishioka, Masafumi Sakashita, Mayumi Tamari, Hideaki Morita, Takeya Adachi

        2022

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    Language:English  

    DOI: 10.1016/j.alit.2022.02.002

  3. More than keratitis, ichthyosis, and deafness: Multisystem effects of lethal GJB2 mutations Reviewed

    Lilly, E., Bunick, C.G., Maley, A.M., Zhang, S., Spraker, M.K., Theos, A.J., Vivar, K.L., Seminario-Vidal, L., Bennett, A.E., Sidbury, R., Ogawa, Y., Akiyama, M., Binder, B., Hadj-Rabia, S., Morotti, R.A., Glusac, E.J., Choate, K.A., Richard, G., Milstone, L.M.

    Journal of the American Academy of Dermatology   Vol. 80 ( 3 ) page: 617 - 625   2019

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jaad.2018.09.042

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  4. Pansclerotic morphea associated with hypohidrosis and anti-M3 muscarinic acetylcholine receptor antibodies Reviewed

    Fujita-Tanaka, H., Ogawa, Y., Muro, Y., Ogawa-Momohara, M., Asashima, H., Tsuboi, H., Sumida, T., Akiyama, M.

    British Journal of Dermatology   Vol. 178 ( 3 ) page: E210 - E211   2018

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

    DOI: 10.1111/bjd.16021

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  5. Survey on patients with undiagnosed diseases in Japan: Potential patient numbers benefiting from Japan's initiative on rare and undiagnosed diseases (IRUD) Reviewed

    Adachi, T., Imanishi, N., Ogawa, Y., Furusawa, Y., Izumida, Y., Izumi, Y., Suematsu, M.

    Orphanet Journal of Rare Diseases   Vol. 13 ( 1 ) page: 208   2018

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1186/s13023-018-0943-y

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  6. Pigmented macules in Waardenburg syndrome type 2 due to KITLG mutation Reviewed

    Ogawa, Y., Kono, M., Akiyama, M.

    Pigment Cell and Melanoma Research   Vol. 30 ( 5 ) page: 501 - 504   2017

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

    DOI: 10.1111/pcmr.12597

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  7. Pityriasis rubra pilaris type v as an autoinflammatory disease by card14 mutations Reviewed International journal

    Takeichi, T., Sugiura, K., Nomura, T., Sakamoto, T., Ogawa, Y., Oiso, N., Futei, Y., Fujisaki, A., Koizumi, A., Aoyama, Y., Nakajima, K., Hatano, Y., Hayashi, K., Ishida-Yamamoto, A., Fujiwara, S., Sano, S., Iwatsuki, K., Kawada, A., Suga, Y., Shimizu, H., Mcgrath, J.A., Akiyama, M.

    JAMA Dermatology   Vol. 153 ( 1 ) page: 66 - 70   2017

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

    Importance: We found CARD14 mutations (2 de novo novel mutations and another previously reported mutation) in 3 of 3 patients with pityriasis rubra pilaris (PRP) type V, but not in patients with PRP of other types. Our findings, combined with the published literature, suggest that type V PRP, both familial and sporadic, can be caused by CARD14 mutations. Detailed clinical observation revealed that all 3 patients displayed unique patchy macular brown hyperpigmentation. Objective: To further determine how often patients with PRP have pathogenic mutations in CARD14 and to elucidate which clinical subtype of PRP is caused by CARD14 mutations. Design, Setting, and Participants: We sequenced the entire coding regions of CARD14 in genomic DNA from patients with 5 clinical subtypes of PRP. The detailed clinical features were analyzed in all the patients. The pathogenicity of each mutation was evaluated by several computational predictions. PRP was classified into 6 subgroups, types I to VI, based on clinical criteria. We categorized all the patients with PRP into the clinical subtypes using the classic PRP classification; 22 cases of PRP with varying subtypes were studied. Main Outcomes and Measures: The prevalence of CARD14 mutations in each subtype of PRP was evaluated. Clinical features and characteristics of patients with PRP with CARD14 mutations were analyzed. Results: Overall 22 patients with PRP were included in our study (12 men, 10 women; mean [SD] age, 26 [18] years). Among 3 patients with PRP type V, all were found to have CARD14 mutations: 2 de novo novel mutations (p.Cys127Ser and p.Gln136Leu), and another previously reported mutation (p.Gly117Ser). All were close to the reported pathogenic domains. In silico analysis of all 3 mutations suggested that they are functionally relevant to pathogenesis. All 3 patients displayed unique patchy macular brown hyperpigmentation additionally to other typical features of PRP. Patients with PRP type I and type IV, 1 patient each, had the rare variants in CARD14. Conclusions and Relevance: Pityriasis rubra pilaris type V is a distinct variant of PRP that is caused by CARD14 mutations. In addition, a rare variant of CARD14 might also be implicated in the pathophysiology of other forms of PRP.

    DOI: 10.1001/jamadermatol.2016.3601

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  8. Image Gallery: Unilaterally dominant acrokeratoelastoidosis (punctate palmoplantar keratoderma type 3) Reviewed

    Taki, T., Ogawa, Y., Sakakibara, A., Kono, M., Akiyama, M.

    British Journal of Dermatology   Vol. 177 ( 4 ) page: E157 - E157   2017

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1111/bjd.15817

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  9. Image Gallery: Palmoplantar hyperkeratosis in dermatomyositis with anti-PM/Scl antibodies Reviewed

    Taki, T., Muro, Y., Ogawa, Y., Akiyama, M.

    British Journal of Dermatology   Vol. 176 ( 5 ) page: E94 - E94   2017

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1111/bjd.15371

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  10. Epstein-barr virus-associated natural killer/T-cell lymphoma in a patient receiving therapy with anti-tumour necrosis factor and thiopurine Reviewed

    Murase, C., Ogawa, Y., Yamamoto, A., Iriyama, C., Akiyama, M.

    Acta Dermato-Venereologica   Vol. 97 ( 2 ) page: 273 - 274   2017

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.2340/00015555-2529

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  11. Biallelic Mutations in KDSR Disrupt Ceramide Synthesis and Result in a Spectrum of Keratinization Disorders Associated with Thrombocytopenia Reviewed

    Takeichi, T., Torrelo, A., Lee, J.Y.W., Ohno, Y., Lozano, M.L., Kihara, A., Liu, L., Yasuda, Y., Ishikawa, J., Murase, T., Rodrigo, A.B., Fernández-Crehuet, P., Toi, Y., Mellerio, J., Rivera, J., Vicente, V., Kelsell, D.P., Nishimura, Y., Okuno, Y., Kojima, D., Ogawa, Y., Sugiura, K., Simpson, M.A., McLean, W.H.I., Akiyama, M., McGrath, J.A.

    Journal of Investigative Dermatology   Vol. 137 ( 11 ) page: 2344 - 2353   2017

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    DOI: 10.1016/j.jid.2017.06.028

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  12. IgE-independent pathophysiology of severe atopic dermatitis demonstrated in an IgE-deficient patient. Reviewed

    Ogawa Y, Kono M, Tsujikawa M, Tsujiuchi H, Akiyama M.

    J Dermatol Sci.   Vol. 82 ( 2 ) page: 139-141   2016.3

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    DOI: 10.1016/j.jdermsci.2016.01.008.

  13. IgE-independent pathophysiology of severe atopic dermatitis demonstrated in an IgE-deficient patient Reviewed

    Ogawa, Y., Kono, M., Tsujikawa, M., Tsujiuchi, H., Akiyama, M.

    Journal of Dermatological Science   Vol. 82 ( 2 )   2016

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    DOI: 10.1016/j.jdermsci.2016.01.008

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  14. Unilateral generalized linear porokeratosis with nail dystrophy Reviewed

    Kono, M., Yokoyama, N., Ogawa, Y., Takama, H., Sugiura, K., Akiyama, M.

    Journal of Dermatology   Vol. 43 ( 3 )   2016

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1111/1346-8138.13204

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  15. Non-infectious panniculitis during hydroxyurea therapy in a patient with myeloproliferative disease Reviewed

    Ogawa, Y., Akiyama, M.

    Acta Dermato-Venereologica   Vol. 96 ( 4 )   2016

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    DOI: 10.2340/00015555-2292

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  16. Design and synthesis of a potent inhibitor of class 1 DYRK kinases as a suppressor of adipogenesis. Reviewed

    Masaki S, Kii I, Sumida Y, Kato-Sumida T, Ogawa Y, Ito N, Nakamura M, Sonamoto R, Kataoka N, Hosoya T, Hagiwara M.

    Bioorg Med Chem.   Vol. 23 ( 15 ) page: 4434-4441   2015.8

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    DOI: 10.1016/j.bmc.2015.06.018.

  17. Anti-PM/Scl antibodies are found in Japanese patients with various systemic autoimmune conditions besides myositis and scleroderma. Reviewed

    Muro Y, Hosono Y, Sugiura K, Ogawa Y, Mimori T, Akiyama M.

    Arthritis Res Ther.   Vol. 17 ( 1 ) page: 57   2015.5

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

    DOI: 10.1186/s13075-015-0573-x.

  18. Anti-PM/Scl antibodies are found in Japanese patients with various systemic autoimmune conditions besides myositis and scleroderma Reviewed

    Muro, Y., Hosono, Y., Sugiura, K., Ogawa, Y., Mimori, T., Akiyama, M.

    Arthritis Research and Therapy   Vol. 17 ( 1 )   2015

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    DOI: 10.1186/s13075-015-0573-x

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  19. Design and synthesis of a potent inhibitor of class 1 DYRK kinases as a suppressor of adipogenesis Reviewed

    Masaki, S., Kii, I., Sumida, Y., Kato-Sumida, T., Ogawa, Y., Ito, N., Nakamura, M., Sonamoto, R., Kataoka, N., Hosoya, T., Hagiwara, M.

    Bioorganic and Medicinal Chemistry   Vol. 23 ( 15 ) page: 4434 - 4441   2015

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:PERGAMON-ELSEVIER SCIENCE LTD  

    Dysregulation of dual-specificity tyrosine-phosphorylation-regulated kinase 1A (DYRK1A) has been demonstrated in several pathological conditions, including Alzheimer's disease and cancer progression. It has been recently reported that a gain of function-mutation in the human DYRK1B gene exacerbates metabolic syndrome by enhancing obesity. In the previous study, we developed an inhibitor of DYRK family kinases (INDY) and demonstrated that INDY suppresses the pathological phenotypes induced by overexpression of DYRK1A or DYRK1B in cellular and animal models. In this study, we designed and synthesized a novel inhibitor of DYRK family kinases based on the crystal structure of the DYRK1A/INDY complex by replacing the phenol group of INDY with dibenzofuran to produce a derivative, named BINDY. This compound exhibited potent and selective inhibitory activity toward DYRK family kinases in an in vitro assay. Furthermore, treatment of 3T3-L1 pre-adipocytes with BINDY hampered adipogenesis by suppressing gene expression of the critical transcription factors PPARc and C/EBPa. This study indicates the possibility of BINDY as a potential drug for metabolic syndrome. (C) 2015 Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.bmc.2015.06.018

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  20. A Palindromic Motif in the -2084 to -2078 Upstream Region is Essential for ABCA12 Promoter Function in Cultured Human Keratinocytes Reviewed

    Yoshitaka Shimizu, Yasushi Ogawa, Kazumitsu Sugiura, Jun-ichi Takeda, Kaori Sakai-Sawada, Teruki Yanagi, Atsushi Kon, Daisuke Sawamura, Hiroshi Shimizu, Masashi Akiyama

    Scientific Reports   Vol. 4   page: 6737   2014.10

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  21. Revertant mutation releases confined lethal mutation, opening Pandora's box: a novel genetic pathogenesis Reviewed

    Ogawa, Y. Takeichi, T. Kono, M. Hamajima, N. Yamamoto, T. Sugiura, K. Akiyama, M.

    PLoS Genet   Vol. 10 ( 5 ) page: e1004276   2014.5

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  22. Establishment of an ELISA to detect anti-glycyl-tRNA synthetase antibody (anti-EJ), a serological marker of dermatomyositis/polymyositis and interstitial lung disease Reviewed

    Hane, H. Muro, Y. Watanabe, K. Ogawa, Y. Sugiura, K. Akiyama, M.

    Clin Chim Acta   Vol. 431   page: 9-14   2014.4

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  23. High survival rate of harlequin ichthyosis in Japan Reviewed

    Shibata, A. Ogawa, Y. Sugiura, K. Muro, Y. Abe, R. Suzuki, T. Akiyama, M.

    J Am Acad Dermatol   Vol. 70 ( 2 ) page: 387-388   2014.2

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  24. Nuclear envelope localization of Ran-binding protein 2 and Ran-GTPase-activating protein 1 in psoriatic epidermal keratinocytes Reviewed

    Yasuda, K. Sugiura, K. Takeichi, T. Ogawa, Y. Muro, Y. Akiyama, M.

    Exp Dermatol   Vol. 23 ( 2 ) page: 119-124   2014.2

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  25. A palindromic motif in the -2084 to -2078 upstream region is essential for ABCA12 promoter function in cultured human keratinocytes Reviewed

    Shimizu, Y., Ogawa, Y., Sugiura, K., Takeda, J.-I., Sakai-Sawada, K., Yanagi, T., Kon, A., Sawamura, D., Shimizu, H., Akiyama, M.

    Scientific Reports   Vol. 4   2014

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    DOI: 10.1038/srep06737

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  26. Revertant Mutation Releases Confined Lethal Mutation, Opening Pandora's Box: A Novel Genetic Pathogenesis Reviewed

    Ogawa, Y., Takeichi, T., Kono, M., Hamajima, N., Yamamoto, T., Sugiura, K., Akiyama, M.

    PLoS Genetics   Vol. 10 ( 5 )   2014

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    DOI: 10.1371/journal.pgen.1004276

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  27. Nuclear envelope localization of Ran-binding protein 2 and Ran-GTPase-activating protein 1 in psoriatic epidermal keratinocytes Reviewed

    Yasuda, K., Sugiura, K., Takeichi, T., Ogawa, Y., Muro, Y., Akiyama, M.

    Experimental Dermatology   Vol. 23 ( 2 )   2014

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1111/exd.12324

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  28. High survival rate of harlequin ichthyosis in Japan Reviewed

    Shibata, A., Ogawa, Y., Sugiura, K., Muro, Y., Abe, R., Suzuki, T., Akiyama, M.

    Journal of the American Academy of Dermatology   Vol. 70 ( 2 )   2014

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jaad.2013.10.055

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  29. Establishment of an ELISA to detect anti-glycyl-tRNA synthetase antibody (anti-EJ), a serological marker of dermatomyositis/polymyositis and interstitial lung disease Reviewed

    Hane, H., Muro, Y., Watanabe, K., Ogawa, Y., Sugiura, K., Akiyama, M.

    Clinica Chimica Acta   Vol. 431   2014

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    DOI: 10.1016/j.cca.2014.01.005

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  30. The majority of generalized pustular psoriasis without psoriasis vulgaris is caused by deficiency of interleukin-36 receptor antagonist Reviewed

    Sugiura, K. Takemoto, A. Yamaguchi, M. Takahashi, H. Shoda, Y. Mitsuma, T. Tsuda, K. Nishida, E. Togawa, Y. Nakajima, K. Sakakibara, A. Kawachi, S. Shimizu, M. Ito, Y. Takeichi, T. Kono, M. Ogawa, Y. Muro, Y. Ishida-Yamamoto, A. Sano, S. Matsue, H. Morita, A. Mizutani, H. Iizuka, H. Muto, M. Akiyama, M.

    J Invest Dermatol   Vol. 133 ( 11 ) page: 2514-2521   2013.11

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  31. Possible roles of barrier-to-autointegration factor 1 in regulation of keratinocyte differentiation and proliferation

    Takama, H. Sugiura, K. Ogawa, Y. Muro, Y. Akiyama, M.

    J Dermatol Sci   Vol. 71 ( 2 ) page: 100-106   2013.8

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  32. Novel ABCA12 missense mutation p.Phe2144Ser underlies congenital ichthyosiform erythroderma Reviewed

    Shimizu, Y. Sugiura, K. Aoyama, Y. Ogawa, Y. Hitomi, K. Iwatsuki, K. Akiyama, M.

    J Dermatol Sci   Vol. 40 ( 7 ) page: 581-582   2013.7

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  33. Novel ABCA12 missense mutation p.Phe2144Ser underlies congenital ichthyosiform erythroderma Reviewed

    Shimizu, Y., Sugiura, K., Aoyama, Y., Ogawa, Y., Hitomi, K., Iwatsuki, K., Akiyama, M.

    Journal of Dermatology   Vol. 40 ( 7 )   2013

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1111/1346-8138.12169

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  34. The majority of generalized pustular psoriasis without psoriasis vulgaris Is caused by deficiency of interleukin-36 receptor antagonist Reviewed International journal

    Sugiura, K., Takemoto, A., Yamaguchi, M., Takahashi, H., Shoda, Y., Mitsuma, T., Tsuda, K., Nishida, E., Togawa, Y., Nakajima, K., Sakakibara, A., Kawachi, S., Shimizu, M., Ito, Y., Takeichi, T., Kono, M., Ogawa, Y., Muro, Y., Ishida-Yamamoto, A., Sano, S., Matsue, H., Morita, A., Mizutani, H., Iizuka, H., Muto, M., Akiyama, M.

    Journal of Investigative Dermatology   Vol. 133 ( 11 ) page: 2514 - 2521   2013

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    Generalized pustular psoriasis (GPP) is a rare inflammatory skin disease that can be life-threatening. Recently, it has been reported that familial GPP is caused by homozygous or compound heterozygous mutations of IL36RN. However, the majority of GPP cases are sporadic and it is controversial whether IL36RN mutations are a causative/predisposing factor for sporadic GPP. We searched for IL36RN mutations in two groups of GPP patients in the Japanese population in this study: GPP without psoriasis vulgaris (PV), and GPP with PV. Eleven cases of GPP without PV (GPP alone) and 20 cases of GPP accompanied by PV (GPP with PV) were analyzed. Surprisingly, 9 out of 11 cases of GPP alone had homozygous or compound heterozygous mutations in IL36RN. In contrast, only 2 of 20 cases of GPP with PV had compound heterozygous mutations in IL36RN. The two cases of GPP with PV who had compound heterozygous mutations in IL36RN are siblings, and both cases had PV-susceptible HLA-A*0206. We determined that GPP alone is a distinct subtype of GPP and is etiologically distinguished from GPP with PV, and that the majority of GPP alone is caused by deficiency of the interleukin-36 receptor antagonist due to IL36RN mutations.

    DOI: 10.1038/jid.2013.230

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  35. Possible roles of barrier-to-autointegration factor 1 in regulation of keratinocyte differentiation and proliferation Reviewed

    Takama, H., Sugiura, K., Ogawa, Y., Muro, Y., Akiyama, M.

    Journal of Dermatological Science   Vol. 71 ( 2 )   2013

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jdermsci.2013.04.007

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  36. A novel IL36RN/IL1F5 homozygous nonsense mutation, p.Arg10X, in a Japanese patient with adult-onset generalized pustular psoriasis Reviewed

    Sugiura, K. Takeichi, T. Kono, M. Ogawa, Y. Shimoyama, Y. Muro, Y. Akiyama, M. Br J Dermatol

    Br J Dermatol   Vol. 167 ( 3 ) page: 699-701   2012.9

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  37. Severe Chilblain Lupus Is Associated with Heterozygous Missense Mutations of Catalytic Amino Acids or their Adjacent Mutations in the Exonuclease Domains of 3'-Repair Exonuclease 1. Reviewed

    Sugiura K, Takeichi T, Kono M, Ito Y, Ogawa Y, Muro Y and Akiyama M

    J Invest Dermatol     page: In press   2012

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  38. Challenges to congenital genetic disorders with "RNA-targeting" chemical compounds Invited Reviewed

    Ogawa Y and Hagiwara M.

    Pharmacol Ther   Vol. 134 ( 3 ) page: 298-305   2012

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  39. Severe chilblain lupus is associated with heterozygous missense mutations of catalytic amino acids or their adjacent mutations in the exonuclease domains of 30-repair exonuclease 1 Reviewed

    Sugiura, K., Takeichi, T., Kono, M., Ito, Y., Ogawa, Y., Muro, Y., Akiyama, M.

    Journal of Investigative Dermatology   Vol. 132 ( 12 ) page: 2855-7   2012

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

    DOI: 10.1038/jid.2012.210

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  40. A novel IL36RN/IL1F5 homozygous nonsense mutation, p.Arg10X, in a Japanese patient with adult-onset generalized pustular psoriasis Reviewed

    Sugiura, K., Takeichi, T., Kono, M., Ogawa, Y., Shimoyama, Y., Muro, Y., Akiyama, M.

    British Journal of Dermatology   Vol. 167 ( 3 )   2012

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1111/j.1365-2133.2012.10953.x

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  41. Challenges to congenital genetic disorders with "RNA-targeting" chemical compounds Reviewed

    Ogawa, Y., Hagiwara, M.

    Pharmacology and Therapeutics   Vol. 134 ( 3 )   2012

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.pharmthera.2012.02.001

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  42. LEDGF/DFS70 activates the MK2/IL6/STAT3 pathway in HaCaT. Reviewed

    Takeichi T, Sugiura K, Muro Y, Ogawa Y, Akiyama M

    J Dermatol Sci   Vol. 63 ( 3 ) page: 203-5   2011.9

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

  43. Leucettines, a class of potent inhibitors of cdc2-like kinases and dual specificity, tyrosine phosphorylation regulated kinases derived from the marine sponge leucettamine B: modulation of alternative pre-RNA splicing. Reviewed

    Debdab M, Carreaux F, Renault S, Soundararajan M, Fedorov O, Filippakopoulos P, Lozach O, Babault L, Tahtouh T, Baratte B, Ogawa Y, Hagiwara M, Eisenreich A, Rauch U, Knapp S, Meijer L, Bazureau JP.

    J Med Chem   Vol. 54 ( 12 ) page: 4172-86   2011.6

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  44. LEDGF/DFS70 activates the MK2/IL6/STAT3 pathway in HaCaT Reviewed

    Takeichi, T., Sugiura, K., Muro, Y., Ogawa, Y., Akiyama, M.

    Journal of Dermatological Science   Vol. 63 ( 3 )   2011

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jdermsci.2011.05.004

    Scopus

  45. Leucettines, a class of potent inhibitors of cdc2-like kinases and dual specificity, tyrosine phosphorylation regulated kinases derived from the marine sponge leucettamine B: Modulation of alternative pre-RNA splicing Reviewed

    Debdab, M., Carreaux, F., Renault, S., Soundararajan, M., Fedorov, O., Filippakopoulos, P., Lozach, O., Babault, L., Tahtouh, T., Baratte, B., Ogawa, Y., Hagiwara, M., Eisenreich, A., Rauch, U., Knapp, S., Meijer, L., Bazureau, J.-P.

    Journal of Medicinal Chemistry   Vol. 54 ( 12 )   2011

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1021/jm200274d

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  46. Overexpression of LEDGF/DFS70 Induces IL-6 via p38 Activation in HaCaT Cells, Similar to that Seen in the Psoriatic Condition. Reviewed

    Takeichi T, Sugiura K, Muro Y, Matsumoto K, Ogawa Y, Futamura K, Kaminuma O, Hashimoto N, Shimoyama Y, Saito H, Tomita Y.

    J Invest Dermatol   Vol. 130 ( 12 ) page: 2760-7   2010.12

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  47. Development of a novel selective inhibitor of the Down syndrome-related kinase Dyrk1A. Reviewed

    Ogawa Y, Nonaka Y, Goto T, Ohnishi E, Hiramatsu T, Kii I, Yoshida M, Ikura T, Onogi H, Shibuya H, Hosoya T, Ito N, Hagiwara M.

    Nature Communications   Vol. 1   2010.10

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

  48. Intravital imaging of IL-1beta production in skin Reviewed

    Matsushima H, Ogawa Y, Miyazaki T, Tanaka H, Nishibu A, Takashima A.

    J Invest Dermatol.   Vol. 130 ( 6 ) page: 1571-1580   2010.6

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

  49. Development of a novel selective inhibitor of the Down syndrome-related kinase Dyrk1A Reviewed

    Ogawa, Y., Nonaka, Y., Goto, T., Ohnishi, E., Hiramatsu, T., Kii, I., Yoshida, M., Ikura, T., Onogi, H., Shibuya, H., Hosoya, T., Ito, N., Hagiwara, M.

    Nature Communications   Vol. 1 ( 7 )   2010

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:NATURE PUBLISHING GROUP  

    Dyrk1A (dual-specificity tyrosine-(Y)-phosphorylation-regulated kinase 1A) is a serine/threonine kinase essential for brain development and function, and its excessive activity is considered a pathogenic factor in Down syndrome. The development of potent, selective inhibitors of Dyrk1A would help to elucidate the molecular mechanisms of normal and diseased brains, and may provide a new lead compound for molecular-targeted drug discovery. Here, we report a novel Dyrk1A inhibitor, INDY, a benzothiazole derivative showing a potent ATP-competitive inhibitory effect with IC50 and K-i values of 0.24 and 0.18 mu M, respectively. X-ray crystallography of the Dyrk1A/INDY complex revealed the binding of INDY in the ATP pocket of the enzyme. INDY effectively reversed the aberrant tau-phosphorylation and rescued the repressed NFAT (nuclear factor of activated T cell) signalling induced by Dyrk1A overexpression. Importantly, proINDY, a prodrug of INDY, effectively recovered Xenopus embryos from head malformation induced by Dyrk1A overexpression, resulting in normally developed embryos and demonstrating the utility of proINDY in vivo.

    DOI: 10.1038/ncomms1090

    Web of Science

    Scopus

  50. Overexpression of LEDGF/DFS70 induces IL-6 via p38 activation in HaCaT cells, similar to that seen in the psoriatic condition Reviewed

    Takeichi, T., Sugiura, K., Muro, Y., Matsumoto, K., Ogawa, Y., Futamura, K., Kaminuma, O., Hashimoto, N., Shimoyama, Y., Saito, H., Tomita, Y.

    Journal of Investigative Dermatology   Vol. 130 ( 12 )   2010

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/jid.2010.203

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  51. Intravital imaging of IL-1Β production in skin Reviewed

    Matsushima, H., Ogawa, Y., Miyazaki, T., Tanaka, H., Nishibu, A., Takashima, A.

    Journal of Investigative Dermatology   Vol. 130 ( 6 )   2010

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/jid.2010.11

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  52. Tissue-specific expression of betaKlotho and fibroblast growth factor (FGF) receptor isoforms determines metabolic activity of FGF19 and FGF21. Reviewed

    Kurosu H, Choi M, Ogawa Y, Dickson AS, Goetz R, Eliseenkova AV, Mohammadi M, Rosenblatt KP, Kliewer SA, Kuro-o M.

    J Biol Chem.   Vol. 282 ( 37 ) page: 26687-26695   2007.9

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  53. Molecular insights into the klotho-dependent, endocrine mode of action of fibroblast growth factor 19 subfamily members. Reviewed

    Goetz R, Beenken A, Ibrahimi OA, Kalinina J, Olsen SK, Eliseenkova AV, Xu C, Neubert TA, Zhang F, Linhardt RJ, Yu X, White KE, Inagaki T, Kliewer SA, Yamamoto M, Kurosu H, Ogawa Y, Kuro-o M, Lanske B, Razzaque MS, Mohammadi M.

    Mol Cell Biol.   Vol. 27 ( 9 ) page: 3417-3728   2007.5

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  54. BetaKlotho is required for metabolic activity of fibroblast growth factor 21 Reviewed

    Ogawa Y, Kurosu H, Yamamoto M, Nandi A, Rosenblatt KP, Goetz R, Eliseenkova AV, Mohammadi M, Kuro-o M.

    Proc Natl Acad Sci U S A.   Vol. 104 ( 18 ) page: 7432-7437   2007.5

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

  55. Molecular insights into the Klotho-dependent, endocrine mode of action of fibroblast growth factor 19 subfamily members Reviewed

    Goetz, R., Beenken, A., Ibrahimi, O.A., Kalinina, J., Olsen, S.K., Eliseenkova, A.V., Xu, C., Neubert, T.A., Zhang, F., Linhardt, R.J., Yu, X., White, K.E., Inagaki, T., Kliewer, S.A., Yamamoto, M., Kurosu, H., Ogawa, Y., Kuro-o, M., Lanske, B., Razzaque, M.S., Mohammadi, M.

    Molecular and Cellular Biology   Vol. 27 ( 9 )   2007

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1128/MCB.02249-06

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  56. βKlotho is required for metabolic activity of fibroblast growth factor 21 Reviewed

    Ogawa, Y., Kurosu, H., Yamamoto, M., Nandi, A., Rosenblatt, K.P., Goetz, R., Eliseenkova, A.V., Mohammadi, M., Kuro-O, M.

    Proceedings of the National Academy of Sciences of the United States of America   Vol. 104 ( 18 )   2007

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1073/pnas.0701600104

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  57. Tissue-specific expression of βklotho and Fibroblast Growth Factor (FGF) receptor isoforms determines metabolic activity of FGF19 and FGF21 Reviewed

    Kurosu, H., Choi, M., Ogawa, Y., Dickson, A.S., Goetz, R., Eliseenkova, A.V., Mohammadi, M., Rosenblatt, K.P., Kliewer, S.A., Kuro-O, M.

    Journal of Biological Chemistry   Vol. 282 ( 37 )   2007

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1074/jbc.M704165200

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  58. HLA-associated production of anti-DFS70/LEDGF autoantibodies and systemic autoimmune disease. Reviewed

    Muro Y, Ogawa Y, Sugiura K, Tomita Y.

    J Autoimmun.   Vol. 26 ( 4 ) page: 252-257   2006.6

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

  59. Regulation of fibroblast growth factor-23 signaling by klotho.

    Kurosu H, Ogawa Y, Miyoshi M, Yamamoto M, Nandi A, Rosenblatt KP, Baum MG, Schiavi S, Hu MC, Moe OW, Kuro-o M.

    J Biol Chem.   Vol. 281 ( 10 ) page: 6120-6123   2006.3

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

  60. Anti-p80 coilin autoantibodies react with a conserved epitope and are associated with anti-DFS70/LEDGF autoantibodies. Reviewed

    Goto N, Sugiura K, Ogawa Y, Watanabe A, Onouchi H, Tomita Y, Muro Y.

    J Autoimmun.   Vol. 26 ( 1 ) page: 42-51   2006.2

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  61. Identification of novel pharmacological activities of an antifungal agent, nystatin, to promote dendritic cell maturation. Reviewed

    Ogawa Y, Mizumoto N, Tanaka H, Matsushima H, Takashima A.

    J Invest Dermatol.   Vol. 126 ( 2 ) page: 349-353   2006.2

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

  62. Anti-p80 coilin autoantibodies react with a conserved epitope and are associated with anti-DFS70/LEDGF autoantibodies Reviewed

    Goto, N., Sugiura, K., Ogawa, Y., Watanabe, A., Onouchi, H., Tomita, Y., Muro, Y.

    Journal of Autoimmunity   Vol. 26 ( 1 )   2006

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jaut.2005.09.001

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  63. Regulation of fibroblast growth factor-23 signaling by Klotho Reviewed

    Kurosu, H., Ogawa, Y., Miyoshi, M., Yamamoto, M., Nandi, A., Rosenblatt, K.P., Baum, M.G., Schiavi, S., Hu, M.-C., Moe, O.W., Kuro-o, M.

    Journal of Biological Chemistry   Vol. 281 ( 10 )   2006

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1074/jbc.C500457200

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  64. Identification of novel pharmacological activities of an antifungal agent, nystatin, to promote dendritic cell maturation Reviewed

    Ogawa, Y., Mizumoto, N., Tanaka, H., Matsushima, H., Takashima, A.

    Journal of Investigative Dermatology   Vol. 126 ( 2 )   2006

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1038/sj.jid.5700081

    Scopus

  65. HLA-associated production of anti-DFS70/LEDGF autoantibodies and systemic autoimmune disease Reviewed

    Muro, Y., Ogawa, Y., Sugiura, K., Tomita, Y.

    Journal of Autoimmunity   Vol. 26 ( 4 )   2006

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jaut.2006.03.005

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  66. Regulation of oxidative stress by the anti-aging hormone klotho. Reviewed

    Yamamoto M, Clark JD, Pastor JV, Gurnani P, Nandi A, Kurosu H, Miyoshi M, Ogawa Y, Castrillon DH, Rosenblatt KP, Kuro-o M.

    J Biol CHem   Vol. 280 ( 45 ) page: 38029-34   2005.11

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

  67. Discovery of novel immunostimulants by dendritic-cell-based functional screening. Reviewed

    Mizumoto N, Gao J, Matsushima H, Ogawa Y, Tanaka H, Takashima A.

    Blood   Vol. 106 ( 9 ) page: 3082-3089   2005.11

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

  68. Discovery of novel immunostimulants by dendritic-cell-based functional screening Reviewed

    Mizumoto, N., Gao, J., Matsushima, H., Ogawa, Y., Tanaka, H., Takashima, A.

    Blood   Vol. 106 ( 9 )   2005

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1182/blood-2005-03-1161

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  69. Regulation of oxidative stress by the anti-aging hormone klotho Reviewed

    Yamamoto, M., Clark, J.D., Pastor, J.V., Gurnani, P., Nandi, A., Kurosu, H., Miyoshi, M., Ogawa, Y., Castrillon, D.H., Rosenblatt, K.P., Kuro-O, M.

    Journal of Biological Chemistry   Vol. 280 ( 45 )   2005

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1074/jbc.M509039200

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  70. Autoantibodies to DFS70/LEDGF are increased in alopecia areata patients. Reviewed

    Okamoto M, Ogawa Y, Watanabe A, Sugiura K, Shimomura Y, Aoki N, Nagasaka T, Tomita Y, Muro Y.

    J Autoimmun.   Vol. 23 ( 3 ) page: 221-231   2004.11

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  71. Autoantigenicity of DFS70 is restricted to the conformational epitope of C-terminal alpha-helical domain. Reviewed

    Ogawa Y, Sugiura K, Watanabe A, Kunimatsu M, Mishima M, Tomita Y, Muro Y.

    J Autoimmun   Vol. 23 ( 3 ) page: 221-231   2004.11

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  72. A case of refractory bullous pemphigoid with plasmapheresis-associated thrombopenia: efficacy of pulsed intravenous cyclophosphamide therapy. Reviewed

    Ogawa Y, Adachi A, Okamoto M, Hashimoto T, Tomita Y.

    J Dermatol.   Vol. 31 ( 8 ) page: 651-654   2004.8

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

  73. A case of refractory bullous pemphigoid with plasmapheresis-associated thrombopenia: Efficacy of pulsed intravenous cyclophosphamide therapy Reviewed

    Ogawa, Y., Adachi, A., Okamoto, M., Hashimoto, T., Tomita, Y.

    Journal of Dermatology   Vol. 31 ( 8 )   2004

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1111/j.1346-8138.2004.tb00571.x

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  74. Autoantigenicity of DFS70 is restricted to the conformational epitope of C-terminal alpha-helical domain Reviewed

    Ogawa, Y., Sugiura, K., Watanabe, A., Kunimatsu, M., Mishima, M., Tomita, Y., Muro, Y.

    Journal of Autoimmunity   Vol. 23 ( 3 )   2004

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1016/j.jaut.2004.07.003

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  75. Autoantibodies to DFS70/LEDGF are increased in alopecia areata patients Reviewed International journal

    Okamoto, M., Ogawa, Y., Watanabe, A., Sugiura, K., Shimomura, Y., Aoki, N., Nagasaka, T., Tomita, Y., Muro, Y.

    Journal of Autoimmunity   Vol. 23 ( 3 ) page: 257 - 66   2004

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

    Alopecia areata (AA) has been suspected to be an autoimmune disease, although there is no distinct evidence, we investigated the relationship between AA and autoantibodies against dense fine speckles 70 kDa (DFS70) in 111 patients with alopecia and 105 healthy controls. The sera from 59 out of 111 (53%) Japanese alopecia patients were positive for anti-nuclear antibody (ANA), as compared to the sera of 16 out of 105 (15%) healthy controls (p < 0.001). Twenty percent (22/111) of the alopecia patients were shown to be positive for the prevalence of anti-DFS70 antibodies, as compared to 8% (8/105) of the healthy controls (p < 0.01). IgG subclass analysis by ELISA showed that IgG1 and IgG2-anti-DFS70 antibodies were dominant in alopecia patients. The DFS70 gene expression in the hair structures was clearly detected in both those with and those without the anti-DFS70 antibody by RT-PCR. Immunohistochemical techniques showed that the DFS70 was localized predominantly in the outer root sheath (ORS) cells. The elevated anti-DFS70 antibodies in alopecia patients and the localization of the DFS70 in the ORS suggest that autoantibodies against the DFS70 are related to the etiology in a certain population of AA.

    DOI: 10.1016/j.jaut.2004.07.004

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    PubMed

  76. The successful use of topical tacrolimus treatment for a chronic actinic dermatitis patient with complications of idiopathic leukopenia. Reviewed

    Ogawa Y, Adachi A, Tomita Y.

    J Dermatol   Vol. 30 ( 11 ) page: 805-809   2003.11

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  77. The Successful Use of Topical Tacrolimus Treatment for a Chronic Actinic Dermatitis Patient with Complications of Idiopathic Leukopenia Reviewed

    Ogawa, Y., Adachi, A., Tomita, Y.

    Journal of Dermatology   Vol. 30 ( 11 )   2003

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1111/j.1346-8138.2003.tb00482.x

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  78. Autoantibody to thioredoxin reductase in an ovarian cancer patient. Reviewed

    Muro Y, Ogawa Y, Kato Y, Hagiwara M.

    Biochem Biophys Res Commun.   Vol. 252 ( 2 ) page: 267-271   1998.1

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  79. Autoantibody to thioredoxin reductase in an ovarian cancer patient Reviewed

    Muro, Y., Ogawa, Y., Kato, Y., Hagiwara, M.

    Biochemical and Biophysical Research Communications   Vol. 242 ( 2 )   1998

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1006/bbrc.1997.7914

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  80. Calmodulin-dependent protein kinase II potentiates transcriptional activation through activating transcription factor 1 but not cAMP response element-binding protein. Reviewed

    Shimomura A, Ogawa Y, Kitani T, Fujisawa H, Hagiwara M.

    J Biol Chem.   Vol. 271 ( 30 ) page: 17957-17960   1996.7

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  81. Calmodulin-dependent protein kinase II potentiates transcriptional activation through activating transcription factor 1 but not cAMP response element-binding protein Reviewed

    Shimomura, A., Ogawa, Y., Kitani, T., Fujisawa, H., Hagiwara, M.

    Journal of Biological Chemistry   Vol. 271 ( 30 )   1996

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    Publishing type:Research paper (scientific journal)  

    DOI: 10.1074/jbc.271.30.17957

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KAKENHI (Grants-in-Aid for Scientific Research) 9

  1. A proof of concept study of medium chain trygryceride diet based treatment for congenital ichtgyosis

    Grant number:17K10206  2017.4 - 2018.3

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    Authorship:Principal investigator 

    Grant amount:\4680000 ( Direct Cost: \3600000 、 Indirect Cost:\1080000 )

  2. Elucidation of roles of lipid mediators in the epidermis to innovate novel therapeutic strategies for keratinization disorders

    Grant number:15H04887  2015.4 - 2018.3

    AKIYAMA Masashi

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    Authorship:Coinvestigator(s) 

    In the present study, we accumulated families with inherited keratinization disorders including ichthyosis, and performed whole exome and/or whole genome sequencing using next generation sequencers to clarify genetic causes of the patients. Clinical information and data from the genetic analysis were collected as our data bank of patients with inherited keratinization disorders.
    To elucidate the interaction between epidermal lipid synthesis and metabolism, and differentiation and proliferation of the epidermal keratinocytes, we analyzed detailed epidermal lipid profiles and differentiation/proliferation statuses of the keratinocytes in our mouse models of inherited ichthyoses. We comprehensively summarized the effects of epidermal functional lipids on differentiation and proliferation of the epidermal keratinocytes. From the present results, we considered novel therapeutic manners for keratinization disorders using epidermal functional lipids and lipid mediators.

  3. Dynamic epigenetic change of keratinocytes in inflammtory skin diseases

    Grant number:26461657  2014.4 - 2018.3

    Yasushi Ogawa

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    Authorship:Principal investigator 

    Grant amount:\4940000 ( Direct Cost: \3800000 、 Indirect Cost:\1140000 )

    This study aimed to investigate the roles of epigenetic changes of keratinocytes in the formation of inflammatory skin lesion of psoriasis. A reverse chemical genomics-approach was adopted. Topical imiquimod-induced skin inflammation was used as a mouse model of psoriasis, and various chemical inhibitors of chromatin modifying enzymes are applied to investigate their effect on the formation of the skin lesion. As a result we newly identified a histone demethylase inhibitor that promote the formation of the lesion, and a kinase inhibitor that suppress the skin lesion.

  4. The disturbed feed forward transcriptional regulation mechanism coupled with disturbed intracellular lipid metabolism in keratinocytes of congenital ichthyosis model mice

    Grant number:25670502  2013.4 - 2015.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Challenging Exploratory Research

    OGAWA Yasushi, SUGIURA Kazumitsu, AKIYAMA Masashi

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    Authorship:Principal investigator 

    Grant amount:\3770000 ( Direct Cost: \2900000 、 Indirect Cost:\870000 )

    This study was designed to verify the hypothesized feed forward mechanism of lipid metabolism-transcriptional regulation in differentiating keratinocytes, and find possible application of this putative mechanism in the treatment of congenital skin diseases. For this purpose we utilized Abca12-deficient as a mouse model of harlequin ichthyosis and CGI-58-deficient mouse as a model of neutral lipid storage disease with ichthyosis. Primary keratinocytes taken from the skin of model mice were treated with agonists of PPAR family nuclear receptors. A PPARγagonist restored the decreased expression of a keratinocyte differentiation marker. It could not, however, provide an overall reversal of the disease phenotype. An attempt to inject of PPAR agonist in utero failed to rescue the early death of newborn mice. Search for skin-specific triglyceride lipase was performed using siRNA targeted at PNPLA family members suggested the putative lipase exists otherwise.

  5. Impact of phosphate toxicity on skin aging

    Grant number:24659527  2012.4 - 2013.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Challenging Exploratory Research

    OGAWA Yasushi

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    Authorship:Principal investigator 

    Grant amount:\3770000 ( Direct Cost: \2900000 、 Indirect Cost:\870000 )

    Hyperphosphatemia is caused by several diseases including chronic renal failure, and is often accompanied by skin manifestations that mimic aging. The "phosphate toxicity" hypothesis suggests that hyperphosphatemia induce aging like symptoms of the body, however, the direct consequence of the high phosphate condition on keratinocytes was not well studied.
    In this study we verified that normal human epidermal keratinocytes (NHEK) are driven into early cellular senescence if cultured under non-optimum phosphate condition. NHEK showed highest population doubling levels (PDL) when cultured in 4 mM phosphate and the concentration lower or higher than this level resulted in decreased PDL. The decrease in PDL was accompanied by increased expression of keratinocyte differentiation markers. No increase in senescence associated secreted proteins was observed. It may be suggested that high phosphate condition may drive NHEK to differentiated state leading to accelerated aging-like phenotype.

  6. Elucidation of epigenetic dysregulation of psoriasis lesions and development of novel therapeutic strategy

    Grant number:23689054  2011.4 - 2015.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Young Scientists (A)

    OGAWA Yasushi, SUGIURA Kazumitsu, AKIYAMA Masashi

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    Authorship:Principal investigator 

    Grant amount:\25090000 ( Direct Cost: \19300000 、 Indirect Cost:\5790000 )

    The present study examined a novel pathogenic mechanism of psoriasis where the epigenetic changes in affected keratinocytes promotes and stabilize the psoriatic skin lesions. The transcription activation cofactor LEDGF shows unique nuclear localization in the proliferating psoriatic keratinocytes. Our study revealed LEDGF shows extranuclear localization in G0/G1 keratinocyte cells, whereas upon stimulation with extracellular growth signals, it translocalizes to the nucleus via MEK and PI3K kinase-mediated mechanism. LEDGF was found to be a H3K36me3 reader, and when localized to the nucleus, it binds to the H3K36me3 motif and recruits the histone modification complex MLL. The present study is in support of the epigenetic model of psoriasis pathogenesis where the nuclear translocalized LEDGF enhances the di- and tri- methylation of H3K4 of the promoter regions of inflammatory cytokines and other psoriasis associated genes, leading to their enhanced and sustained expression.

  7. Investigation of two-step theory involved with TIF1-gamma in cancer-associated with dermatomyositis

    Grant number:23591618  2011.4 - 2015.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    MURO YOSHINAO, SUGIURA Kazumitsu, OGAWA Yasushi

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    Authorship:Coinvestigator(s) 

    The pathogenic mechanisms has been still unknown in cancer-associated dermatomyositis (CADM). We investigated whether malignant tissues in CADM have the aberrant expression of TIF1-γ, which is a serological marker of CADM, and also investigated the possibility of interaction between TIF1-γ, and TGFβand other associated molecules. We showed the high expression of TIF1-γ
    in malignant tissues in patients with anti-TIF1-γ and suggested the possibility of tumor growth by the phosphorylation of STAT3 through IL-6.

  8. Innovation of novel treatments for various phenotypes of ichthyosis by restoration of ABCA12 lipid transporter gene expression

    Grant number:23249058  2011.4 - 2014.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (A)

    AKIYAMA Masashi, OGAWA Yasushi, KONO Michihiro, ABE Riichiro, SUGIURA Kazumitsu, MURO Yoshinao

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    Authorship:Coinvestigator(s) 

    In the present study, we established ABCA12-mutant mice harboring ABCA12 partial loss-of-function mutations, as model mice for congenital ichthyosiform erythroderma. In the model mice, we evaluated the up-regulation effects on ABCA12 gene expression by various compounds, which were expected to have up-regulation effects on ABCA12 gene expression. As for the compounds which were proved to have up-regulation effects on ABCA12 gene expression, we further investigated treatment efficacy of the up-regulators of ABCA12 gene expression in the model mice, by monitoring ichthyosis phenotype recovery and restoration of skin barrier function.
    In addition, we also established model mice carrying ABCA12 loss-of-function mutations as a model of harlequin ichthyosis. Using the model mice, we evaluated treatment efficacy of various read-through compounds to harlequin ichthyosis phenotypes by monitoring restoration of the stratum corneum barrier function and phenotype recovery.

  9. Molecular Mechanism of Chemotherapy Resistance of Malignant Melanoma

    Grant number:23659548  2011 - 2012

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Challenging Exploratory Research

    OGAWA Yasushi

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    Authorship:Principal investigator 

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

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Industrial property rights 2

  1. DYRKを阻害するベンゾチアゾール誘導体を含有する医薬組成物

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    Applicant:萩原 正敏、 澁谷 浩司、 大西 英理子、 小川 靖、細谷 孝充、 平松 俊行、 吉田 実代

    Application no:2008-190277  Date applied:2008.7

    Country of applicant:Domestic  

  2. FGF21 Upregulates Expression of GLUT-1 in a βKlotho-Dependent Manner.

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    Applicant:Kuro-o M, Ogawa Y, Kurosu H, Rosenblatt K

    Application no:U.S. Patent Number: 7,537,903 

    Date registered:2009.5 

    Country of applicant:Foreign country