Basic Medicine, Molecular and Cellular Biology, Immunology

Molecular and Cellular Biology

Let's Enjoy Science Together!

Medical Sciences Course

  • Master / Doctoral Degree

Faculty

HORIUCHI, HisanoriHORIUCHI, Hisanori
HORIUCHI, Hisanori

Professor, M.D. Ph.D.

*Concurrent Position

Research Theme

  • Intracelluar signaling escpecially focusing on small GTPases
  • Innate immunity escpecially focusing on NET-formation of neutrophils
  • Research on hemostasis and thrombosis (anti platelet therapy and acquired von Willebrand syndrome)
Research Keywords:

ral, mTOR, neutrophil NETs, protein citrullination, acquired von Willebrand syndrome

Technical Keywords:

biochemistry, molecular biology, cell biology , mouse biology, multimer analysis of von Willebrand factor

Laboratory Introduction

We have investigated molecular and cellular biology/medicine focusing on small GTPases by identifying critical molecules. Recently we have identified Munc13-4 as a Rab27 effector and RalGAPs, negative regulators of small GTPase Ral implicated in endo- and exocytosis and tumorigenesis. So, let's join us and enjoy science to have your own molecules/projects.
We have focused on following projects:
1. To elucidate the evaluating system of cellular nutrition by focusing of small GTPase regulating mTOR pathway.
2. To elucidate molecular mechanism of NET formation of neutrophils, which is implicated in not only host defense but also thrombosis, cancer metastasis and autoimmune diseases.
3. Clinically, we are evaluating heart disease-related acquired von Willebrand syndrome with bleeding tendency by multimer analysis of von Willebrand factors.

Figure 1. The functions and regulatory mechanism of a small GTPase Ral

Figure 1. The functions and regulatory mechanism of a small GTPase Ral

Figure 2. RalGAP and its suppressing role of cancer metastasis

Figure 2. RalGAP and its suppressing role of cancer metastasis

Recent Publications

  • R. Shirakawa*, H. Horiuchi (2015) Ral GTPases: Crucial Mediators of Exocytosis and Tumorigensis.( a review) J Biochem (Tokyo) in press
  • N. Yaoita, R. Shirakawa, Y. Fukumoto, K. Sugimura, S. Miyata, Y. Miura, K. Nochioka, M. Miura, S. Tatebe, T. Aoki, S. Yamamoto, K. Satoh, T. Kimura, H. Shimokawa, H. Horiuchi* (2014) Platelets are highly activated in patients of chronic thromboembolic pulmonary hypertension (CTEPH) Arteriosclerosis Thromb Vasc Biol, 34, 2486-2494
  • R Saito, R Shirakawa, H Nishiyama*, T Kobayashi, M Kawato, T Kanno, K Nishizawa, Y Matsui, T Ohbayashi, M Horiguchi, T Nakamura, T Ikeda, K Yamane, E Nakayama, E Nakamura, Y Toda, T Kimura, T Kita, O Ogawa, H Horiuchi* (2013) Downregulation of Ral GTPase-activating-protein causes tumor invasion and metastasis of bladder cancer. Oncogene 32, 894-902
  • Y. Murata, T. Yasumi*, R. Shirakawa, K. Izawa, H. Sakai, J. Abe, N. Tanaka, T. Kawai, K. Oshima, M. Saito, R. Nishikomori, O. Ohara, E. Ishii, T. Nakahata, H. Horiuchi*, T. Heike (2011) Rapid diagnosis of familial hemophagocytic lymphohistiocytosis type 3 (FHL3) by flow cytometric detection of intraplatelet Munc13-4 protein. Blood 118, 1225-1230
  • R. Shirakawa, S. Fukai, M. Kawato, T. Higashi, H. Kondo, T. Ikeda, E. Nakayama, K. Okawa, O. Nureki, T. Kimura, T. Kita, H. Horiuchi* (2009) Tuberous sclerosis tumor suppressor complex-like complexes act as GTPase activating proteins for Ral GTPases. J. Biol. Chem., 284, 21580-21588.