教員紹介

SDGsへの取り組み

最終学歴

大阪大学大学院　医学研究科　博士課程修了
（病理系・分子発生生物学専攻）

取得学位

博士（医学）（大阪大学）

所属学会

日本発生生物学会、日本分子生物学会

現在の専門分野

脳神経科学、器官発生学、病因病態学

現在の研究課題

●モワット・ウィルソン症候群の原因遺伝子Sip1の神経系における機能解析
●腎臓形成におけるSip1の発現と機能

主要研究業績

●マウス胚の原腸陥入と脊索形成に関与する転写因子の同定
●モワット・ウィルソン症候群の原因遺伝子であるSip１の脳神経系における発現と機能

最近の研究業績

1. Shukunami, C., Takimoto, A., Nishizaki, Y., Yoshimoto, Y., Tanaka, S., Miura, S., Watanabe, H., Sakuma, T., Yamamoto, T., Kondoh, G., Hiraki, Y. Scleraxis is a transcriptional activator that regulates the expression of Tenomodulin, a marker of mature tenocytes and ligamentocytes. Sci Rep. 8 (1): 3155 (2018)

2. Rasouly HM, Kumar S, Chan S, Pisarek-Horowitz A, Sharma R, Xi QJ, Nishizaki Y, Higashi Y, Salant DJ, Maas RL, Lu W. Loss of Zeb2 in mesenchyme-derived nephrons causes primary glomerulocystic disease. Kidney Int. Dec; 90 (6):1262-1273 (2016)

3. Takagi T, Nishizaki Y, Matsui F, Wakamatsu N, Higashi Y. De novo inbred heterozygous Zeb2/Sip1 mutant mice uniquely generated by germ-line conditional knockout exhibit craniofacial, callosal and behavioral defects associated with Mowat-Wilson syndrome. Hum Mol Genet. 24 (22): 6390-6402 (2015)

4. Nishizaki, Y., Takagi, T., Matsui, F., Higashi, Y. SIP1 expression patterns in brain investigated by generating a SIP1-EGFP reporter knock-in mouse. Genesis. 52 (1):56-67 (2014)

5. Takimoto, A., Nishizaki, Y., Hiraki, Y., Shukunami, C. Differential actions of VEGF-A isoforms on perichondrial angiogenesis during endochondral bone formation. Dev. Biol. 332: 196-211 (2009)

6. Yukata, K., Matsui, Y., Shukunami, C., Takimoto, A., Goto, T., Nishizaki, Y., Nakamichi, Y., Kubo, T., Sano, T., Kato, S., Hiraki, Y., Yasui, N. Altered fracture callus formation in chondromodulin-I deficient mice. Bone. 43 (6):1047-1056 (2008)

7. Shukunami, C., Takimoto, A., Miura, S., Nishizaki, Y., Hiraki, Y. Chondromodulin-I and tenomodulin are differentially expressed in the avascular mesenchyme during mouse and chick development. Cell Tissue Res. 332 (1): 111-122 (2008)

8. Mori, H., Shukunami, C., Furuyama, A., Notsu, H., Nishizaki, Y., Hiraki, Y. Immobilization of bioactive fibroblast growth factor-2 into cubic proteinous microcrystals (Bombyx mori cypovirus polyhedra) that are insoluble in a physiological cellular environment. J. Biol. Chem. 282 (23): 17289-17296 (2007)

9. Sawada, A., Nishizaki, Y., Sato, H., Yada, Y., Nakayama, R., Yamamoto, S., Nishioka, N., Kondoh, H., Sasaki, H. Tead proteins activate the Foxa2 enhancer in the node in cooperation with a second factor. Development 132 (21): 4719-4729 (2005)

10. Setoguchi, K., Misaki, Y., Kawahata, K., Shimada, K., Juji, T., Tanaka, S., Oda, H., Shukunami, C., Nishizaki, Y., Hiraki, Y., Yamamoto, K. Suppression of T cell responses by chondromodulin-I, a cartilage-derived angiogenesis inhibitory factor: therapeutic potential in rheumatoid arthritis. Arthritis Rheum. 50 (3): 828-839 (2004)

11. Nakamichi, Y., Shukunami, C., Yamada, T., Aihara, K., Kawano, H., Sato, T., Nishizaki, Y., Yamamoto, Y., Shindo, M., Yoshimura, K., Nakamura, T., Takahashi, N., Kawaguchi, H., Hiraki, Y., Kato, S. Chondromodulin-I is a bone remodeling factor. Mol. Cell. Biol. 23 (2): 636-644 (2003)

12. Nishizaki, Y., Shimazu, K., Kondoh, H., Sasaki, H. Identification of essential sequence motifs in the node/notochord enhancer of Foxa2 (Hnf3beta) gene that are conserved across vertebrate species. Mech. Dev. 102 (1-2): 57-66 (2001)

13. Sasaki, H., Nishizaki, Y., Hui, C., Nakafuku, M., Kondoh, H. Regulation of Gli2 and Gli3 activities by an amino-terminal repression domain: implication of Gli2 and Gli3 as primary mediators of Shh signaling. Development. 126 (17): 3915-3924 (1999)

14. Ding, Q., Fukami, S., Meng, X., Nishizaki, Y., Zhang, X., Sasaki, H., Dlugosz, A., Nakafuku, M., Hui, C. Mouse suppressor of fused is a negative regulator of sonic hedgehog signaling and alters the subcellular distribution of Gli1. Curr. Biol. 9 (19): 1119-1122 (1999)