General Description of the DepartmentOur main researches have been dealing with Human Immunodeficiency virus (HIV) and Hepatitis C Virus (HCV), both of which affect a considerable population worldwide. In addition to anti-viral drug screening, we conduct immunological and molecular biological experiments.
We also study Chediak-Higashi syndrome, a rare genetic disease that manifests immunological defects and abnormal pigmentation of the skin, hair and eyes. Mechanisms of the disease development and means of chemotherapy are investigated.
Two oncological researches have started: one exploring the functions of p63 (a member of the tumor suppressor p53 family), and the other concerning the transcriptional control of human endogenous retrovirus-K (HERV-K).
Profile of the Faculty MembersProfessor: Masahiko ITO, M.D. & Ph.D.
Area of Interest:
(1) Mechanism of induction in long term non-progressors infected with HIV
(2) Study of immunotherapy against infectious diseases and cancers.
(3) Study of prevention and treatment of HIV infection in the developing countries
Associate Professor: Iyoko KATOH, Ph.D.
Area of Interest:
(1) Functions of p63 (TP63) in squamous cell carcinoma development.
(2) Structure, function and regulation of HERV-K LTR.
Assistant Professor: Atsuya Yamashita, Ph.D.
Area of Interest:
(1) Discovery and development of anti-HCV agents.
(2) Molecular mechanism of HCV replication.
Assistant Professor: Hirotake KASAI, Ph.D.
Area of Interest:
(1) Molecular biology of the Chediak-Higashi syndrome
(2) Immunological responses to health-care mushroom extracts.
Assistant Professor: Li-Min HE, M.D. & Ph.D.
Area of Interest:
(1) Cytokine induction by HIV.
(2) Anti-HCV drug screening
Research Activities
(1) HCV
We focused on screening a set of licensed drugs which have not been recommended previously for antiviral use. As a result, we found that griseofulvin (anti fungal agent) and bisphosphonate (anti osteoporosis agents ) had a suppressive effect on HCV replication assessed using the HCV subgenomic replicon system.
(2) Future possibility of chemotherapy for Chediak-Higashi syndrome (CHS).
A thiol proteinases inhibitor, E-64-d, was found to improve the functional defects of polymorphonuclear cells and natural killer cells in test tubes.
(Int Immunopharmacol. 2009 Mar;9(3):366-70; Int Immunopharmacol. 2007 Jul;7(7):973-80).
(3) Identification of the target genes of p63.
Nuclear protein p63 (TP63) acts as a transcriptional activator to regulate proliferation and differentiation of normal keratinocytes and squamous cell carcinomas. Our study uncovered that ITGA3 coding for integrin alpha3 and MFGE8 for Milk Fat Globule-EGF Factor 8 (MFG-E8) are activated by p63. We suggested a new concept that p63 controls cell fate through induction of cell adhesion molecules.
(J Biol Chem. 2004, 279(48):50069-77; Oncogene. 2008, 10;27(3):308-17)
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