Bulletin of the Medical Research Institute

Advanced Molecular Medicine
Molecular Medicine and Metabolism
Prof. Yoshihiro OGAWA
Molecular Pharmacology
Prof. Masaki NODA
Molecular Cell Biology
Prof. Hiroshi SHIBUYA
Molecular Neuroscience
Prof. Kohichi TANAKA
Cell Regulation
Prof. Yuji YAMANASHI
Bio-informational Pharmacology
Prof. Tetsushi FURUKAWA
Autonomic Physiology
Prof. Yoshifumi KATAYAMA
●
Molecular Medicine and Metabolism
Professor
Associate Professor
Assistant Professor
Yoshihiro OGAWA
Yasutomi KAMEI
Takayoshi SUGANAMI
Our mission is to elucidate the molecular basis of and to develop the therapeutic strategies against
the metabolic syndrome, the coexistence of several risk factors for atherosclerosis, including
visceral obesity, hyperglycemia, atherogenic dyslipidemia, and hypertension. Accordingly, we have
been focusing on the pathophysiologic and therapeutic implications of adipocytokines, nuclear
hormone receptors, and transcriptional co-activators/co-repressors in the metabolic syndrome.
―Research projects―
Preadipocytes Mature
● Pathophysiologic and therapeutic implications of adipocytokines (leptin, TNF-α, free fatty acids
adipocytes
etc.)
● Pathophysiologic and therapeutic implications of chronic, low-grade inflammation in the
metabolic syndrome
● Molecular mechanisms of adipocyte proliferation and differentiation
● Pathophysiologic and therapeutic implications of nuclear hormone receptors, transcriptional
co-activators/co-repressors
Measurement of % body
● Molecular genetics of congenital metabolic disorders
fat, muscle mass, and
bone density
―Publications―
A. Yasoda et al. Overexpression of CNP in chondrocytes rescues achondroplasia through a MAPK-dependent pathway.
Nat. Med. 10: 80-86, 2004.
E. Suganami et al. Leptin stimulates ischemia-induced retinal neovascularization: possible role of vascular endothelial
growth factor expressed in retinal endothelial cells. Diabetes 53: 2443-2448, 2004.
Y. Kamei et al. Skeletal muscle FOXO1 (FKHR)-transgenic mice have less skeletal muscle mass, down-regulated type I
(slow twitch/red muscle) fiber genes. J. Biol. Chem. 279: 41114-41123, 2004.
T. Suganami et al. Prevention and reversal of renal injury by leptin in a new mouse model of diabetic nephropathy. FASEB
J. 19:127-129, 2005.
Genetically obese ob/ob
mice (left) and lean
littermates (right)
1
MRI 2005
homepage：http://www.tmd.ac.jp/mri/prm/index.html
contact：Yoshihiro Ogawa (ogawa.mmm@mri.tmd.ac.jp)
locarion：Surugadai area, 5th floor
● Molecular
Pharmacology
Professor
Lecturer
Lecturer
Masaki NODA
Yoichi EZURA
Kazuhisa NAKASHIMA
To clarify the molecular mechanism for the pathogenesis of major diseases affecting skeletal
system (ex, osteoporosis, osteoarthrosis and rheumatoid arthritis), we examine the abnormality in
mineral homeostasis or calcium metabolism, cellular responses, and cytokine network affecting the
etiological bases for those diseases.
Bone Mass Analysis
―Research projects―
● Transcription factors regulating bone cell differentiation
● Cytokines and growth factors
● Mechanical stress and cell attachment
● Developmental biology on bone and cartilage
―Publications―
Morinobu M, Noda M, et al.: The nucleocytoplasmic shuttling protein CIZ reduces adult bone mass by inhibiting bone
morphogenetic protein induced bone formation. J. Exp. Med. 201(6):, 961-970 (2005)
Elefteriou F, Noda M,et al.: Leptin regulation of bone resorption by the sympathetic nervous system and CART. Nature
Osteocyte Net Work
434:514-520 (2005)
Usui M, Noda M,et al.: Tob deficiency superenhances osteoblastic activity after ovariectomy to block estrogen
deficiency-induced osteoporosis. Proc. Natl. Acad. Sci. USA 101( 17):6653-6658 (2004)
Yumoto K, Noda M, et al.: Osteopontin deficiency protects joints against destruction in anti-type II collagen
antibody-induced arthritis in mice. Proc. Natl. Acad. Sci. USA 99(7):4556-61 (2002)
Bone Loss Signaling
●
Molecular Cell Biology
homepage：http://www.tmd.ac.jp/mri/mph/index.html
contact：Masaki NODA (noda.mph@mri.tem.ac.jp)
location ： Surugadai area, 7・8th floor
Professor
Associate Professor
Assistant Professor
Lecturer
Hiroshi SHIBUYA
Junji OHNISHI
Kiyotoshi SATOH
Tetsuo MORIGUCHI
Morphogenesis and organogenesis of the vertebrate are regulated by various signaling molecules inducing the cell-growth
and differentiation. The failure of many these signal molecules has also been achieved with induction of the diseases.
Therefore, the elucidation of signal transduction network regulating generation and differentiation becomes an important
problem upon clarifying the mechanism of morphogenesis, organogenesis and diseases. We focus the signal transduction
network regulating the mechanisms of morphogenesis and organogenesis in developmental process.
―Research projects―
● Signal transduction mechanism, which controls the cell proliferation and differentiation.
● Analysis of signaling molecules, which regulate the development and differentiation using the model animals.
―Publications―
Ohkawara, B., et al.: Role of the TAK1-NLK-STAT3 pathway in TGF-β-mediated mesoderm induction. Genes Dev. 18,381-386 (2004).
Hyodo-Miura, J. et al.: Involvement of NLK and Sox11 in neural induction in Xenopus development. Genes Cells 7, 487-496 (2002).
Nishita, M. et al.: Interaction between Wnt and TGF-β signalling pathways during formation of Spemann's organizer. Nature 403, 781-785 (2000).
homepage：http://www.tmd.ac.jp/mri/mri-mcb/index_j.html
contact：Hiroshi SHIBUYA (shibuya.mcb@mri.tmd.ac.jp)
location ： Surugadai area, Bldg. 3, 3rd・４th floor
2
MRI 2005
● Molecular
Neuroscience
Professor
Associate Professor
Assistant Professor
Kohichi TANAKA
Hiroko OHKI-HAMAZAKI
Michihiro MIEDA
The final goal of our research is to understand molecular, cellular, and neuronal ensemble
mechanisms underlying higher order brain functions including learning and memory. For that
purpose, we combine molecular genetics, physiological and behavioral methods. The laboratory
also studies the mechanism that underlies neuronal cell death and regeneration.
Epilepsy in glutamate
transporter
knockout
mice
―Research projects―
● Role of astrocyte-neuron interactions in higher brain function
● Role of glutamate transporters in the brain
● Role of neuropeptides in higher brain function (bombesin receptors and orexin)
● Neural basis of learning and memory in avian model
―Publications―
Apparatus for the imprinting
behavior
Sleep/wake
cycles
of
transgenic and wild-type
mice
● Cell
Maekawa F. et al.: Leptin resistance and enhancement of feeding facilityation by melanin-concentrating hormone in
mice lacking bombesin receptor subtaype-3. Diabetes 53, 570-576 (2004).
Mieda M, et al.: Orexin peptides prevent cataplexy and improve wakefulness in orexin neuron-ablated model of
narcolepsy in mice. Proc. Natl. Acad. Sci. USA. 101, 4649-4654 (2004).
Voutsinos-Porche B. et al.: Glial glutamate transporters mediate a functional metabolic crosstalk between neurons and
astrocytes in the mouse developing cortex. Neuron 37, 275-2846 (2003)
homepage : http://www.tmd.ac.jp/mri/aud/index.html
contact ： Kohochi TANAKA (tanaka.aud@mri.tmd.ac.jp)
location ： Yushima area, Bldg. 3, 3rd floor
Regulation
Professor
Associate Professor
Assistant Professor
Yuji YAMANASHI
Osamu HIGUCHI
Ryuichi MASHIMA
The major interest is in molecular signals regulating a variety of cellular activities,
aiming to address how deregulated cellular signals cause neoplastic, immune, neural,
infectious, and developmental diseases.
We currently study the molecular
mechanisms of such signaling events through experiments with cultured cells, model
animals, and clinical samples.
Role of the Dok proteins.
―Research projects―
● Roles of Dok-family adaptors in cellular signaling
● Identification of novel signaling molecules downstream of protein-tyrosine kinases
● Roles of signaling molecules in embryogenesis and muscle differentiation.
● Mechanisms of protein-tyrosine kinase-mediated tumorigenesis.
―Publications―
Novel signaling molecules
Mouse model system
3
MRI 2005
Shinohara H, Inoue A, ---, & Yamanashi Y.: Dok-1 and Dok-2 are negative regulators of
lipoplysaccharide-indcued signaling. J. Exp. Med. 201, 333-339 (2005)
Yasuda T, Shirakata M, ---, & Yamanashi Y.: Role of Dok-1 and Dok-2 in myeloid homeostasis and
suppression of leukemia. J. Exp. Med. 200, 1681-1687 (2004)
Imadome K, Shirakata M, ---, & Yamanashi Y.: CD40 ligand is a critical effector of Epstein-Barr virus in host
cell survival and transformation. Proc. Natl. Acad. Sci. USA. 100, 7836-7840 (2003)
dok
Yamanashi Y, Tamura T, ---, & Baltimore D.: Role of the rasGAP-associated docking protein p62 in
negative regulation of B cell receptor-mediated signaling. Genes Dev. 14, 11-16 (2000)
homepage ： http://www.tmd.ac.jp/mri.creg/index.html
contact ： Yuji YAMANASHI (yamanashi.creg@mri.tmd.ac.jp)
location ： Yushima area, Bldg. 3, 3rd floor
● Bio-informational
Pharmacology
Professor
Assistant Professor
Tetsushi FURUKAWA
Junko KUROKAWA
We study function and structure of ion channels and transporters from both physiological and molecular
approaches, with collaboration with bio-informatics, structural biology, and organic chemistry. Our aims
are to establish a novel strategy for prevention and treatment of common cardiovascular diseases, such
as arrhythmias and heart failure．
―Research projects―
● Gender-specific medicine for sudden death and lethal arrhythmias
（Single-channel recording by
● Personalized medicine for sudden death and lethal arrhythmias
patch-clamp technique）
● Cardiac channelopathy (LQT, Brugada syndrome, etc.)
● Discovery of leads/seeds and drugs for lifestyle-related diseases in tranditional medicines
(kannpo・herbs etc.) and natural foods (isoflavone・saponin etc.)
● Establishment of novel cardiac regeneration system and autograft system
Functional study
―Publications―
Bio-informatics
（ion channel structure）
Cardiomyocyte regeneration
（Cell transplantation in animal
models）
● Autonomic
Bai CX, Kurokawa J, Furukawa T, et al.: Non-genomic regulation of cardiac repolarization currents by testosterone.
Circulation in press (2005).
Bai CX, Kurokawa J, Furukawa T, et al.: Role of nitric oxide in Ca2+-sensitivity of the delayed rectifier K+ current in
cardiac myocytes. Circ. Res. 96, 64-72 (2005).
Kurokawa J, Kass RS, et al.:Regulatory action of the A-kinase anchoring protein Yotiao on a heart potassium channel
downstream of PKA phosphorylation. Proc. Natl. Acad. Sci. USA 101, 16374-16378 (2004).
Marx SO, Kurokawa J, et al.: Requirement of a macromolecular signaling complex for β-adrenergic receptor
modulation of the KCNQ1-KCNE1 potassium channel. Science 295, 496-499 (2002).
homepage：http://www.tmd.ac.jp/mri/cph/index.html
contact：Tetsushi FURUKAWA (t_furukawa.bip@mri.tmd.ac.jp)
location: Surugadai area, 6・8th floor
Professor
Associate Professor
Research Associate
Physiology
Yoshifumi KATAYAMA
Keiji HIRAI
Eiichiro KANDA
Autonomic functions are essentially involved in maintaining the “homeostasis”.
Mechanisms underlying the regulation of the autonomic functions are investigated at
intracellular, cellular, tissue and organ levels by using the electrophysiological method
together with optical, immunocytochemical and molecular biological techniques.
Glutamate release from
the growth cones
―Research projects―
● Cellular culture of autonomic sensory neurons and analysis of electrophysiological
properties and chemosensitivities of their growth cones.
● Electrophysiological and immunocytochemical studies on functional organization of the
enteric nervous system.
● Comparative studies on actions of endogenous and food-related bioactive substances
on gut functions.
● Electrophysiolgical and immunocytochemical studies of actions of sleeping-feeding
neuropeptides on the autonomic functions
―Publications―
Electrophysiological
effects of orexin-A and B
on an enteric neuron.
Katayama Y, Homma T, Hara Y & Hirai K: Tea catechin, (-)-epigallocatechin gallate, facilitates cholinergic
ganglion transmission in the myenteric plexus of the guinea-pig small intestine. Neurosci Lett 319, 63-66
(2002).
Soeda H, Tatsumi,H., Katayama,Y et al.: Functional characterization of calcium channels localized on the
growth cones of cultured rat dorsal root ganglion cells. Neurosci Lett 325, 5-8 (2002).
Katayama Y, Homma T, Honda K & Hirai K: Actions of orexin-A in the myenteric plexus of the guinea-pig small
intestine. NeuroReport 14, 1515-1518 (2003).
Katayama Y, Hirai K et al.: Actions of orexins on individual myenteric neurons of the guinea-pig ileum:
orexin-A or-B? NeuroReport, 16, 745-749 (2005).
homepage：http://www.tmd.ac.jp/mri/auto/index_j.html
contact：Yoshifumi KATAYAMA (kataauto@tmd.ac.jp)
location ： Surugadai area, 2nd floor
4
MRI 2005
Pathophysiology
Neuropathology
Prof. Hitoshi OKAZAWA
Pathological Biochemistry
Prof. Hirobumi TERAOKA
Developmental and Regenerative Biology
Prof. Hiroshi NISHINA
Criminal Psychiatry
Prof. Akira YAMAGAMI
Immunology
Prof. Takeshi TSUBATA
Molecular Pathogenesis
Prof. Akinori KIMURA
Virus Research Unit
Associate Prof. Norio SHIMIZU
● Neuropathology
Transcriptome analysis of
polyQ diseases
Professor
Associate Professor
Assistant Professor
COE Research Associate
Hitoshi OKAZAWA
Yasushi ENOKIDO
Kazuhiko TAGAWA
Mei-lingQI
Our goals in research are elucidation of molecular mechanisms of neurodegenerative disorders
(especially, polyglutamine diseases, Alzheimer’s diseases and motor neuron diseases) and
development of novel therapeutics of those intractable disorders.
―Research projects―
● Transcriptome and proteome analyses of neurodegeneration
● Development and analysis of animal models of neurodegnerative disorders
● Analysis of nuclear dysfunction in neurodegeneration and molecular definition of
neurodegeneration
● Understanding of molecular basis of intelligence
● Analysis of molecular mechanism of neural stem cell differentiation
―Publications―
PQBP1disease
Drosophila model
Oct-3/4 in neural
stem cells
5
MRI 2005
Okazawa H., Rich T., Chang A., Lin X., Waragai M., Kajikawa M., Enokido Y., Komuro A., Kato S. Shibata M., Hatanaka
H., Mouradian M.M., Sudol M., Kanazawa I. (2002) Interaction between mutant ataxin-1 and PQBP-1 affects transcription
and cell death. Neuron 34, 701-713.
Okuda T., Hattori H., Takeuchi S., Shimizu J., Ueda H., Palvimo J.J., Kanazawa I., Kawano H.., Nakagawa M., Okazawa
H. (2003) PQBP-1 transgenic mice show a late-onset motor neuron disease phenotype. Human Mol. Genet. 12,
711-725.
Okazawa H, Okamoto K, Ishino, F, Ishino-Kaneko T, Takeda S, Toyoda Y,
Muramatsu M and Hamada H (1991) The oct-3 gene, a gene for an embryonic transcription factor, is controlled by a
retinoic acid repressible enhancer. EMBO J. 10, 2997-3005.
Okamoto K, Okazawa H, Okuda A, Sakai M, Muramatsu M and Hamada H (1990) A novel octamer binding
transcription factor is differentially expressed in mouse embryonic cells. Cell 60, 461-472.
homepage：http://www.tmd.ac.jp/mri/npat/index.html
contact： Hitoshi OKAZAWA (okazawa.npat@mri.tmd.ac.jp)
location ： Yushima area, Bldg. 3, 7th floor
● Pathological
IR/drugs, S-phase
DSB
Ku
(p70/p86)
DNA-PK
(p470)
DNA ligase IV
XRCC4
？
Molecular mechanism
of NHEJ
Biochemistry
Professor
Assistant Professor
Hirobumi TERAOKA
Kinji ASAHINA
In relationship between cell fate and DNA metabolism, we examine molecular mechanism of
NHEJ in DNA double-strand break repair and hepatocyte differentiation from extrahepatic origins
including ES cells and cord blood cells for clinical application.
―Research projects―
● Repair of DNA double-strand breaks by nonhomologous end-joining
● Regulation of cellular function by PI3K-related protein kinases (DNA-PK, ATM, ATR)
● Epigenetic expression of hepatocyte-related and hepatocyte-specific genes
● Hepatocyte differentiation from embryonic stem (ES) cells, and isolation/expansion
● Hepatic differentiation from umbilical cord blood cells, and for clinical application
―Publications―
Shibata A, et al.: Parp-1 deficiency causes an increase of deletion mutations and insertions /rearrangements in vivo
after treatment with an alkylating agent. Oncogene 24,1328-1337 (2005)
Asahina K, et al.: Expression of the liver-specific gene Cyp7a1 reveals hepatic differentiation in embryoid bodies
derived from mouse embryonic stem cells. Genes Cells 9, 1297-1308 (2004)
Kakinuma S, et al.: Human umbilical cord blood as a source of transplantable hepatic progenitor cells. Stem Cells 21,
217-227 (2003)
Chinzei R, et al.: Embryoid-body cells derived from an mouse embryonic stem cell line show differentiation capacity into
functional hepatocytes. Hepatology 36, 22-29 (2002)
homepage：http://www.tmd.ac.jp/mri/pbc/hyousi.html
contact：Hirobumi TERAOKA (hteraoka.pbc@mri.tmd.ac.jp)
location ： Surugadai area, 3rd・4th floor
Hepatocyte differentiation
from extrahepatic origins
● Developmental
and Regenerative Biology
Professor
Assistant Professor
Hiroshi NISHINA
Teiji WADA
We are studying physiological roles of stress signaling pathways in organ formation and
regeneration using knockout mice, and are identifying signaling pathways regulating liver formation
and function using Medaka mutants. Furthermore, we are trying to establish a cell therapy for
intractable diseases such as liver failures using self-bone marrow cells.
Fig. 1
Defective liver formation
Fig. 2
Signaling pathways
―Research projects―
● Physiological roles of the SAPK/JNK signaling pathway in organ development and
regeneration in mice
● Signaling pathways that regulate liver formation and function in Medaka
● Establishment of model organisms for human diseases
● Establishment of a cell therapy for liver failures using self bone marrow cells
―Publications―
Wada T, et al.: The molecular scaffold Gab2 is a critical component of RANK signaling and
osteoclastogenesis. Nat. Med.11, 394-399 (2005).
Wada T, et al.: MKK7 couples stress signaling to G2/M cell cycle progression and cellular senescence.
Nat Cell Biol. 6, 215-226 (2004).
Watanabe T, et al.: Mutations affecting liver development and function in Medaka, Oryzias latipes,
screened by multiple criteria. Mech. Dev. 121, 791-802 (2004).
Nishitai G, et al.: Stress induces mitochondria-mediated apoptosis independent of SAPK/JNK activation in
ES cells. J. Biol. Chem. 279, 1621-1626 (2004).
Fig. 3
Medaka as a model organism
for human diseases
homepage：http://www.tmd.ac.jp/dbio/index.html
contact：Hiroshi NISHINA (nishina.dbio@mri.tmd.ac.jp)
location ： Yushima area, Bldg. 3, 3rd・4th floor
6
MRI 2005
● Criminal
Psychiatry
Unravel Crime, Behavior disorder, Victimization
and find out Strategy of Treatment and Prevention
Improve Mental Health of the Society
Minimize Crime and Victimization
Establish
standard
assessment
tool for Risk
Accumulate
and Analyze
Data of
Mentally
Disordered
Offenders
Evidencebased new
treatment
strategy for
PTSD
Effective
treatment
program for
sex offenders
Accumulate
and Analyze
Data of Sex
Offenders
Treatment of
serious PTSD
cases and
evaluation of
the effect
Establish Research Center
for Forensic Mental Health
Professor
Associate Professor
Akira YAMAGAMI
Shugo OBATA
We unravel crime, juvenile delinquency, behavior disorder and trauma of victims
psychiatrically, and try to find out methods of treat and prevent them. This
department is expected to be a leading center of forensic psychiatry in Japan, and
was given special fund for the research projects written below from Ministry of
Education, Science.
―Research projects―
● Analysis of risk factors concerning to the violence of mentally disordered
offenders, and establishing the assessment standard to evaluate the risk.
● Evaluation and classification of sex offenders, and development of new
treatment program for them.
● Establishment of evidence-based new treatment strategy for PTSD of crime
victims.
―Publications―
Akira Yamagami: How to treat mentally disordered offenders? Gendaikeijihou. No.44:24-29, 2002,
Akira Yamagami, Fumiko Anada: Psychology of victims of crime and Support for them. Horei
Publication, 2001, Dussich J.P.J., Friday P.C., Okada T., Yamagami A.& Knudten D.:Different
Response to Violence in Japan and America. pp201, Criminal Justice Press, USA, 2001,
homepage：http://www.tmd.ac.jp/mri/mri-crps/index_j.html
contact：Taeko Hagiwara (hagiwara.crps@mri.tmd.ac.jp)
location：Surugadai area, 6th floor
● Immunology
Professor
Associate Professor
Assistant Professor
Takeshi TSUBATA
Takahiro ADACHI
Kozo WATANABE
We investigate basic mechanisms of immune responses by focusing on lymphocyte apoptosis
and carbohydrate signals and we attempt to establish novel strategies for controlling
autoimmunity, allergy and infection based on the new paradigm.
A normal cell
and an apoptotic cell
Cell signaling analysis
(Intracellular Ca2+ mobilization)
Immunohistological analysis
(Lymphoid architecture of spleens)
7
MRI 2005
―Research projects―
● Investigation of the mechanisms that maintain the normal humoral immune system which is
not induced by self antigens or environmental antigens respond to pathogenic
microorganisms
● Investigation of the mechanisms of vaccination and immunological memory of host defense
by vaccination induced immune memory
● Elucidation of the function of carbohydrate signals in immune responses
● Establishment of novel strategies for controlling autoimmunity and allergy
● Establishment of novel strategies for host defense against microorganisms
―Publications―
Nitschke, L. and Tsubata, T. (2004): Molecular interactions regulate BCR signal inhibition by CD22 and CD72. Trends
Immunol. 25: 543-550.
Wakabayashi, C., Adachi, T., Wienands, J. and Tsubata, T. (2002): A distinct signaling pathway used by the
IgG-containing B cell antigen receptor. Science 298: 2392-2395.
Higuchi, T., Aiba, Y., Nomura, T., Matsuda, J., Mochida, K., Suzuki, M., Kikutani, H., Honjo, T., Nishioka, K. and
Tsubata T. (2002): Cutting Edge: Ectopic expression of CD40 ligand on B cells induces lupus-like autoimmune
disease. J. Immunol. 168: 9-12.
homepage：http://www.tmd.ac.jp/mri/imm/HP/index.html
contact：Takeshi TSUBATA （tsubata.imm@mri.tmd.ac.jp）
location：Yushima area, Bldg. 2, 5th floor
● Molecular
I
1
II
- 1 -
+3 -
- 2+
- 2 - +3-
Pathogenesis
+4-
- 5+
4
SCD
III
+1 -
+2-
-3 -
- 4+
Genetic analysis of
multiplex family
GFPGFP-WT
488nm
YFPYFP-Mut
514nm
GFPGFP-WT
488nm
488nm
10mm
10mm
merge
YFPYFP-Mut
514nm
10mm
merge
F
10mm
Functional analysis of
disease-related genes
SL
MI
SL CAD
SL
0.0
logP (2xｎ)
-1.0
-2.0
-3.0
∼0.7 Mb
-4.0
-6.0
∼3.2 Mb
within 0.9Mb
-5.0
∼4.9 Mb
MS334
∼1.1 Mb
within 0.4Mb
128Ser
128Arg
leukocyte
Genome-wide approach and
functional analysis of CAD
Akinori KIMURA
Michio YASUNAMI
Takuro ARIMURA
To develop new strategies for curative treatments of various cardiovascular diseases
(cardiomyopathy, arrhythmia and coronary atherosclerosis) and immune-related diseases
(insulin-dependent diabetes mellitus, autoimmune thyroiditis, rheumatoid arthritis and Takayasu
disease), we identify and analyze the human genome diversities involved in the etiology and
pathogenesis of the diseases. In addition, genome diversities of immune-related genes are
investigated to obtain a new strategy for developing vaccines.
―Research projects―
● Identification and functional analysis of novel disease genes for idiopathic cardiomyopathy and
idiopathic ventricular arrhythmia
● Functional modification of disease-related molecules
● Genome-wide approach to identify the disease gene for coronary disease
● Genome diversity of immune-related genes in immune response
―Publications―
Hayashi T, et al: TCAP mutations in hypertrophic cardiomyopathy and dilated cardiomyopathy. J Am Col Cardiol 44;
2192-2201 (2004)
Ueda K, et al: Functional characterization of a trafficking-defective HCN4 mutation, D553N, associated with cardiac
arrhythmia. J Biol Chem 279; 27194-27198 (2004)
Arimura T, et al: A Cypher/ZASP mutation associated with dilated cardiomyopathy alters the binding affinity to protein
kinase C. J Biol Chem 279: 6746-6752 (2004)
Matano T, et al: Cytotoxic T lymphocyte-based control of simian immunodeficiency virus replication in a preclinical
AIDS vaccine trial, J Exp Med 199: 1709-1718(2004)
homepage：http://www.tmd.ac.jp/mri/m-path/index.html
contact：Akinori KIMURA (akitis@mri.tmd.ac.jp)
location：Surugadai area, 3rd・4th floor
Frontier Research Unit
- Virus Research Unit
●
Professor
Associate Professor
Assistant Professor
Associate Professor
Assistant Professor
Norio SHIMIZU
Masaki SHIRAKATA
As refractory virus infections are serious problems for congenital or acquired immunocompromised
hosts, development of new treatment techniques and new anti-viral drugs are urgent problems to
solved. The goals of our research unit are the elucidation of development mechanisms of EB virus
infections, the employment of immunodeficiency animals for the creation of virus research models
and investigating the practicality of utilizing adoptive immunotherapy for the treatment of virus
infections and malignant carcinomas.
―Research projects―
T cell therapy
(Center for cell therapy） ● Treatment of refractory virus infections and malignant carcinomas through the use of adoptive
immunotherapy using activated T lymphocytes.
● Development of new exhaustive laboratory tests for viruses which can be used in quality checks
of cellular preparations used in cell therapy and regenerative medicine as well as clinical
inspections.
● Employment of immunodeficiency mice for AIDS model research in the development of new
AIDS drugs.
Development of new
AIDS drugs
● Analysis of the development mechanisms of EB virus infections.
―Publications―
30
25
F DC L C
p2 4 ( n g / m l)
20
15
10
Fib r o bla s t（ HF L 1)
5
0
FD C L C + マ ン ナ ン
M O L T4 の み
-5
Oyoshi M.K., Nagata H., Kimura N., et al. Preferential expansion of Vgamma9-JgammaP/Vdelta2 -Jdelta3 gamma delta
T-cells in nasal T-cell lymphoma and chronic active Epstein-Barr virus (EBV) infection. Am.. J. Patol.162, 1629-1638
(2003)
Nagata H., Konno A., Kimura N., et al.: Characterization of novel natural killer (NK) and gamma/delta T-cell lines
established from primary lesions of nasal T/NK cell lymphomas associated with Epstein-Barr virus. Blood 97, 708-713
(2001).
Shimizu N., Sekine T., K.Ito et al.: Large-scale ex vivo expansion of primary T-lymphocyte in late-stage AIDS patients.
AIDS. Res. Hum. Retroviruses 16, 611-612(2000).
Analysis of EBV
homepage： http://www.tmd.ac.jp/mri/mri-vir/index.html,
http://www.tmd.ac.jp/grad/cct1/
contact：Norio SHIMIZU (nshivir@mri.tmd.ac.jp)
location ： Yushima area, Bldg. 2, 4th floor
8
MRI 2005
Medical Genomics
Molecular Cytogenetics
Prof. Johji INAZAWA
Molecular Genetics
Prof. Yoshio MIKI
Molecular Epidemiology
Prof. Masaaki MURAMATSU
Biochemical Genetics
Prof. Shigetaka KITAJIMA
Functional Genomics
Prof. Masatoshi HAGIWARA
Epigenetics
Prof. Fumitoshi ISHINO
Bioinformatics
Prof. Hiroshi TANAKA
Redox Response Cell Biology
Assoc. Prof. Shun-ichi KURATA
● Molecular
Cytogenetics
Professor
Associate Professor
Assistant Professor
HTDFRP Associate Professor
Johji INAZAWA
Issei IMOTO
Sana YOKOI- ISHIHARA
Ken-ici OZAKI
Our goal is to establish personalized medicine in human diseases including cancer and genetic
diseases by the integrated genome approach in the post-sequence era. For this purpose, we
examine genomic copy-number aberrations using custom-made tools, analyze gene
expression systematically, and explore epigenetically dysregulated genes and functional DNA
elements.
Genomic analysis of
cancer using CGH-array
Diagnosis of genetic
disease using CGH-array
Genome-wide screening
of methylated sequence
by BAMCA
9
MRI 2005
―Research projects―
● Identification and characterization of genes involved in carcinogenesis
● Identification and functional analyses of genes related to genetic diseases
● Development of genomic micro-arrays and their application for analyses of cancer and
genetic diseases
● Development of novel methods for diagnosis and therapy of cancer and genetic diseases
―Publications―
Izumi H, et al: Frequent silencing of DBC1 is by genetic or epigenetic mechanisms in non-small cell lung cancers.
Hum. Mol. Genet. 14, 997-1007 (2005)
Yokoi S, et al: Amplification and overexpression of SKP2 are associated with metastasis of non-small- cell lung
cancers to lymph nodes. Am. J. Pathol. 165, 175-80 (2004)
Imoto I, et al: Identification of ZASC1 encoding a Kruppel-like zinc finger protein as a novel target for 3q26
amplification in esophageal squamous cell carcinomas. Cancer Res. 63, 5691-6 (2003)
homepage：http://www.tmd.ac.jp/mri/cgen/framepage.html
contact：Johji INAZAWA (johinazcgen@mri.tmd.ac.jp)
location：Yushima area, Bldg. 3, 6th floor
● Molecular
Genetics
Professor
Assistant Professor
COE Program Lecturer
Yoshio MIKI
Kiyotsugu YOSHIDA
Yuki HAMANO
Our purpose is Basic biological research which clarifies the biological nature of cancer and
establishing new diagnosis and medical treatment of the cancer based on the information
acquired by the research. Concretely, we analyze the roles of DNA damage repair and
apoptosis in carcinogenesis, focusing on some kinases which bear this signal transduction, or
BRCA1 and BRCA2.
Subcellular localization of
BRCA2
―Research projects―
● The investigation of a mechanism in breast carcinogenesis
• Functional analysis of the gene responsible for hereditary breast cancer, BRCA2
• Development of the personalized medicine for breast cancer applying genome science
● The intracellular signaling transduction and cell death in DNA damage
• Analysis of the cell cycle control mechanism by protein kinase C delta
• The investigation of the mechanism of apoptosis induction by c-Abl
―Publications―
Clustering analysis
Yoshida K, Yamaguchi T, Natsume T, Kufe D, Miki Y: JNK phosphorylation of 14-3-3- regulates nuclear targeting of
c-Abl in the apoptotic response to DNA damage. Nat. Cell Biol. 7, 278-285 (2005)
Yoshida K, Miki Y: Role of BRCA1 and BRCA2 as regulators of DNA repair, transcription, and cell cycle in response
to DNA damage. Cancer Sci. 95, 866-871 (2004)
Morotomi-Yano K, Yano K, Saito H, Sun Z, Iwama A, Miki Y: Human relatory factor X4 (RFX4) is a testis-specific
dimeric DNA-binding protein that cooperates with other human RFX memberes. J. Biol. Chem. 277, 836-842
(2002)
homepage：http://www.tmd.ac.jp/mri/mgen/index.html
contact：Yoshio MIKI (miki.mgen@mri.tmd.ac.jp)
location：Yushima area, Bldg. 3, 6th floor
c-Abl 核内移行モデル
A model of c-Abl
transfer to nucleous
● Molecular
Epidemiology
Professor
Assistant Professor
Masaaki MURAMATSU
Tomomi KIMURA
We are interested in the study of discovering the genetic cause of the diseases, which leads
the primary prevention, molecular diagnosis, and development of new medicine in the near
future. In addition to the environmental and lifesyle factors, we focus on the inherited
personal differencies, such as SNPs (single nucleotude polymorphisms).
SNP typing
―Research projects―
● Individual difference of the susceptibilities of diseases dependent on the polymorphisms
● Genetic difference between the responders and non-responders for the drug therapies
● Bioinformatics using polymorphisms and haplotypes
―Publications―
Araki J, Ohashi J, Muramatsu M: Application of discordant sib-pair linkage analysis for mapping minor
histocompatibility antigen loci in a novel graft-vs-host-disease model. Tissue Antigens 64, 243-50 (2004)
Kitano H, Oda K, Kimura T, Matsuoka K, Csete M, Doyle J, Muramatsu M: Metabolic syndrome and robustness
tradeoffs. Diabetes 53 (Suppl 3), S6-S15 (2004)
Kimura T, Yokoyama T, Matsumura Y, Yoshiike N, Date C, Muramatsu M, Tanaka H: NOS3 genotype dependent
correlation between blood pressure and physical activity. Hypertension 41, 355-360 (2003)
Haplotype and promoter activity
homepage：http://www.tmd.ac.jp/mri/epi/index.html
contact：Masaaki MURAMATSU (muramatsu/epi@mri.tmd.ac.jp)
location：Surugadai area, 9th floor
10
MRI 2005
● Biochemical
Genetics
Promoter clearance
IIo
IIa
IIB
TBP
TATA
IIF
IIE
IIH
Ini
P-TEFb
Holoenzyme
IIo
IIa
Stall
Ini
IIa
Shigetaka KITAJIMA
Yujiro TANAKA
Mimi TAMAMORI-ADACHI
Our group studies on basic mechanism of Pol II transcription, structure and biological function of
specific transcription factors, and re-activation of cell cycle of terminally-differentiated cardiac cells,
thus aiming to develop novel therapy of disease.
Preinitiation complex (PIC)
IIB
IIF
TBP
TATA
Professor
Associate Professor
Assistant Professor
FCP1
IIF
Termination
polyA
& RecyclingIIo
―Research projects―
● Basic mechanism of Pol II transcription cycle from elongation, termination and recycling
● Histone methylation and chromatin regulation
● Cell fate-determining activity of bZip-type transcription factor ATF3
● Cell cycle reactivation of terminally differentiated cardiac cells
Elongation
ElonginA
IIF
Transcription cycle
by RNA polymerase
c-myc+/+
c-myc-/-
BrdU
DAPI
A2
merge
―Publications―
c-myc+/+
Tamura K, et al: Stress response gene ATF3 is a target of c-myc in serum-induced cell proliferation. EMBO J. revised
Kip1
promotes cell proliferation of rat neonatal cardiomyocytes
Tamamori-Adachi M, et al: Down-regulation of p27
induced by nuclear expression of cyclin D1 and CDK4. J. Biol. Chem. 279, 50429-50436 (2004)
Yamazaki K, et al: Mammalian Elongin A Is not essentual for cell viability but required for proper cell-cycle progression
with limited alteration of gene expression. J. Biol. Chem. 278, 13585-13589 (2003)
Yamazaki Y, et al: Identification and characterization of a novel transcription elongation factor elongin A3. J. Biol.
Chem. 277, 26444-26451 (2002)
Hashimoto Y, et al: An alternatively spliced isoform of transcriptional repressor ATF3 and its induction by stress stimuli.
Nucleic Acids Res. 30, 2398-2406 (2002)
Cai Y, et al: Homocysteine-responsive ATF3 gene expression in human vascular endothelial cells: activation of c-Jun
NH2-terminal kinase and promoter response element. Blood 96, 2140-2148 (2000)
c-myc-/-
A2
Cross-talk regulation of
ATF3 and c−Myc in cell
第一の障害サイクリンD1の核内発現障害
増殖刺激
G1
S
G0
第二の障害
p27の分解障害
Ｍ
G2
homepage ： http://www.tmd.ac.jp/mri/bgen/open.html
contact ： Shigetaka KITAJIMA (kita.bgen@mri.tmd.ac.jp)
location： Yushima area, Bldg. 3, 6th floor
Reactivation cell cycle of
cardiomyocytes
● Functional
SR proteins
Genomics
DNA
Transcription
Pre-mRNA
Phosphorylation
Dephosphorylation
m7G
RNA splicing
Other processing
EJC
Mature
(A) n mRNA
Nuclear pore
Export
Translation
m7G
(A) n
mRNA Processing
Professor
Associate Professor
Lecturer
Assistant Professor
Masatoshi HAGIWARA
Tetsuro HIROSE
Hidehito KUROYANAGI
Takeshi FUKUHARA
We are studying mechanisms by which genome-encoded information become functional;
how the fate of primary transcripts are determined, how the RNAs are processed exported
out of the nucleus and how their quality is controlled. We are also developing drugs that
can modulate the function of such regulation systems and applying them to the clinical
aspect.
―Research projects―
● Development and application of SR protein kinase inhibitors.
● Processing and quality control mechanisms of cellular RNAs.
● Mechanisms of tissue-specific alternative splicing in vivo.
● in vitro transcription-splicing coupling system.
● CREB (cAMP response element binding protein) signals in C. elegans dauer formation.
―Publications―
RFP
GFP
DIC
In vivo monitoring system of
tissue-specific alternative splicing
11
MRI
2005
Muraki M, et al: Manipulation of alternative splicing by a newly developed inhibitor of Clks. J. Biol. Chem. 279,
24246-24254 (2004)
Katsu R, et al: Novel SR-related protein Clasp specifically interacts with inactivated Clk4 and induces the
exon EB inclusion of Clk. J. Biol. Chem. 277, 44220-44228 (2002)
Nagai Y, et al: A fluorescent indicator for visualizing cAMP-induced phosphorylation in vivo. Nat. Biotechnol.
18, 313-316 (2000)
homepage：http://www.tmd.ac.jp/mri/mri-end/index.html
contact：Masatoshi HAGIWARA (m.hagiwara.end@mri.tmd.ac.jp)
location：Yushima area, Bldg. 3, 5th floor
● Epigenetics
Professor
Lecturer
Fumitoshi ISHINO
Takashi KOHDA
From the viewpoint of genomic function, we study inheritance, development and
evolution by genetical and epigenetical approaches. By understanding genomic function
Peg of mammals including human, we would like to contribute to establish “new human
biology and medicine” in the 21th century.
―Research projects―
● Genomic imprinting in mammals (There is a very good biological reason for having
Meg
both father and mother for everyone.)
● Somatic cloned animals (Genetic identity does not necessarily mean that cloned
Genomic imprinting
animals are the same as donor animals.)
● Evolution of mammalian genomic function (Genetic evidence indicates relationship
between changes of genomic function and evolution of living organism.)
―Publications―
Mouse embryo at
12.5dpc
Shiura H et al: Meg1/Grb10 overexpression causes postnatal growth retardation and insulin resistance via
negative modulation of the IGF1R and IR cascades. Biochem. Biophys. Res. Commun. 329, 909-916
(2005)
Suzuki S et al: Genomic imprinting of IGF2, P57KIP2 and PEG1/MEST in a marsupial, thetammar wallaby.
Mechanisms of Develop. 122, 213-222 (2005)
Ono R et al: Identification of a large novel imprinted gene cluster on mouse proximal chromosome 6.
Genome Res. 13, 1696-1705 (2003)
Kaneko-Ishino T et al: The regulation and biological significance of genomic imprinting in mammals. J.
Biochem. (Review) 133, 699-711 (2003)
homepage：http://www.tmd.ac.jp/mri/epgn/index.html
contact：Fumitoshi ISHINO (fishino.epgn@mri.tmd.ac.jp)
location：Surugadai area, 5th floor
Professor
Associate Professor
Adjunct Professor
Adjunct Associate Professor
● Bioinformatics
Hiroshi TANAKA
Yoshito MIIMURA
Hiroshi MIZUSHIMA
Fengrong Ren
We study the challenges in life science and medicine from the points of view to understand
life and disease as an unified system. In life science, we are trying to build a new field which
might be called “systems evolutionary biology”. In medical field, we are engaged in
developing systems pathology based on the comprehensive clinical omics.
olfactory receptor evolution
C11
C02
A04
A17
A11
A08
A14
A12
B11
B01
B02
B07
B16
B09
B15
B18
C08
C05
C16
C01*1
C09*1
C06*2
C04*2
HIV within-host evolution
―Research projects―
● Molecular evolution of olfactory receptor multigene family.
● Analysis of the evolutionary process of within-host HIV and prediction of anti-HIV drug
resistance by bioinformatics approaches.
● Systems evolutionary biology: evolutionary analysis of Hox developmental
systems.
● Ubiquitous medicine, systems pathology of cancer.
―Publications―
Niimura, Y. Nei, M: From The Cover: Evolutionary dynamics of olfactory receptor genes in fishes and tetrapods.、
Proc. Natl. Acad. Sci. USA 102, 6039-6044 (2005)
Ogishima S, Gojobori T, Tanaka H: Missing-link in the evolution of Hox clusters (submitting)
F. Ren, S. Ogishima, H. Tanaka: Longitudinal phylogenetic tree of within-host viral evolution from
noncontemporaneous samples: a distance-based sequential-linking method. Gene, 317, 89-95 (2003)
Hox cluster evolution
homepage：http://bioinfo.tmd.ac.jp
contact：Hiroshi TANAKA (tanaka@cim.tmd.ac.jp)
location：Yushima area, Bldg. 2, 5th floor
12
MRI
2005
● Frontier
Research Unit
-Redox Response Cell Biology
Associate Professor
Shun-ichi KURATA
Our research aims to understand molecular mechanisms mediating diverse cellular responses to oxidative stress, as well
as to approach redox system failure causing various diseases by chemical biology.
―Research Projects―
● The newly identified apoptosis-inducing mechanism inside the mitochondria by physiological redox stress. (See the pathway
indicated by bold arrows in the Figure.)
● Cellular signal transduction pathways and transcriptional regulation in response to oxidative stress: the NF-κB and
MAPK cascades.
● Functions of p63, a p53 family protein, in epithelial tissue development and carcinogenesis: trans-activation of genes for
cell adhesion and migration.
Apoptosis-inducing pathways in mitochondria
Cytochrome c
∆ψm
ATP
ADP
Outer membrane
Inner membrane
Inner membrane
damage
Matrix
Physiological oxidative stress
Pro-apoptotic
Bcl-2 family proteins
Outer membrane
permeability
transition
∆ψm-low
Bcl-2
―Publications―
∆ψm-hypo
∆ψm
Cytochrome c
released
Procaspase-9
Apaf-1
Caspase-9
Bcl-2
Activated caspase-9
released
Procaspase-3
Dimerization
S
S
Katoh I, Tomimori Y, Ikawa Y, Kurata S: Dimerization and processing of
procaspase-9 by redox stress in mitochondria. J. Biol. Chem., 279, 15515-15523,
(2004)
Kurata S et al: p51/p63 controls subunit α3 of the major epidermis integrin
anchoring the stem cells to the niche. J. Biol. Chem. 279, 50069-50077 (2004)
Kurata S: Selective activation of p38 MAPK cascade and mitotic arrest caused
by low level oxidative stress. J. Biol. Chem. 275, 23413-23416 (2000)
Outer
membrane
traffic
ｃontact：
Shun-ichi KURATA
contact：Shun-ichi
KURATA(kushbgen@mri.tmd.ac.jp)
(kushbgen@tmd.ac.jp)
location：Yushima
area,
Bldg.
3,
5th floor
location：Yushima area, Bldg. 3, 5th floor
Caspase-3
Caspase cascade
Apoptosis
Project Research Unit
●
access（e-mail or homepage）
Assoc. Prof. Tatsuro IKEUCHI
Assoc. Prof. Seiko KAWANO
http://www.tmd.ac.jp/TMDU/mri/mri-card
Assoc. Prof. Michinori KUBOTA
Assoc. Prof. Toshihiko KUROIWA
http://www.tmd.ac.jp/mri/npat/kuroiwa/index.html
Assoc. Prof. Shinobu SAKAMOTO
Assoc. Prof. Yuji HIRANO
hirano.card@mri.tmd.ac.jp
Assoc. Prof. Saburo HORIKAWA
hori-pbc@mri.tmd.ac.jp
Assoc. Prof. Tokio YAMAGUCHI
toki.bgen@mri.tmd.ac.jp
Assist. Prof. Toshiko OGATA
Assist. Prof. Shuji SASA
Assist. Prof. Hisae HORI
hisae-h.tis@mri.tmd.ac.jp
Assist. Prof. Noriko YAMAGUCHI
noriko-y.tis@mri.tmd.ac.jp
13
MRI
2005
Division of Integrative Science
● Pathogenetic regulation：under construction
● Biosystem Generation ：under construction
Professor
Assistant Professor
Assistant Professor
● Neurotraumatology
Superficial recording of γ oscillation
during POCR session (super‐imposed)
Toshinori NAKAMURA
Keiji HASHIMOTO
Kazuma ISHIMATSU
The aim of our research is to elucidate the mental health status and the needs of victims
including traffic accident survivors and their family members. We also intend to develop the
psycho-medical and psycho-social approach to support the victims, especially the
psychological technique in psychiatry and/or rehabilitational medicine for the people with
higher brain dysfunction from traumatic brain injury. The department was funded by the
General Insurance Association of Japan and was established in 2003.
―Research projects―
● Psycho-medical aspects of rehabilitations for the victims of traumatic brain injury, and the
proper intervention for its issues.
● Psycho-social aspects of family members of the victims of traumatic brain injury, and the
proper intervention for its issues
―Publications―
rt. hemisphere
lt. hemisphere
The γ oscillation was represented predominantly on right frontal lobes.
lobes.
Nakamura T, et al.: Prefrontal cortex will be responsible for the cognitive integration of visual features, - as to a
case of frontal dementia reversible during nootropic treatment. The Int J of Neuropsychopharmacology,
3(Suppl.1): S355, 2000
Nakamura T,, et al.: Prefrontal γ oscillation mediated a new cognitive rehabilitation intervention ( POCR ) for
TBI and brain-damaged patients psychosocial human growth. SfN abstract2004. 11
Nakamura T, et al.: ADEQUATE PAIN RELIEF AND IMMEDIATE MENTAL CARE FOR PATIENTS WITH
TRAUMATIC BRAIN INJURY IMPROVE PATIENT’S WELL-BEING AND QUALITY OF LIFE. J Trauma, 2005
in submission.
homepage：http://www.tmd.ac.jp/mri/crps/neuro_trauma/index.html
contact：Toshinori NAKAMURA (naka.crps@mri.tmd.ac.jp)
location：Surugadai area, 6th floor
● School of Biomedical Science
― Structural Biology
Professor
Associate Professor
Nobutoshi ITO
Teikichi IKURA
We study structural and physicochemical features of biopolymers (especially proteins) by X-ray
crystallography and other techniques to elucidate their function at atomic resolution. Such information
is hoped to help understanding diseases and designing small molecules, potentially leading to new
drugs. We also contribute to maintenance and development of the database for the protein structures
as a member of the PDBj (Protein Data Bank Japan).
―Research projects―
● Structural analysis of SR protein kinases and their interactions with small ligands
● Physicochemical analysis of the functions of peptidyl-prolyl cis/trans isomerases
● Study of in vivo protein folding on the basis of structural analysis of trigger factor
―Publications―
X-ray crystallography
(upper: the barnase- barstar
complex, lower: the active site
of a catalytic antibody)
Westbrook J, Ito N, Nakamura H, Herick K, Berman HM: PDBML: the representation of archival
macromolecular structure data in XML. Bioinformatics 21, 988-992 (2005)
Ikura T, Urakubo Y, Ito N: Water-mediated interaction at a protein-protein interface. Chem. Phys. 307,
111-119 (2004)
Ito N, Sakamoto H, Kobayashi K, Kaneta Y, Kawaguchi Y, Ohkawa T, Nakamura H: New features of
PDBj-ML, an XML format for protein data bank. Genome Informatics 13, 488-489 (2002)
Higo J, Ito N, Kuroda M, Ono S, Nakajima N, Nakamura H: Energy landscape of a peptide consisting of α-helix,
31-helix, β-turn, β-hairpin, and other disordered conformations. Protein Sci. 10, 1160-1171 (2001)
contact：Nobutoshi ITO (ito.str@tmd.ac.jp)
location：Yushima area common research bldg. 2nd floor
14
MRI 2005
Organization
Medical Research
Institute
Devision of Advanced
Molecular Medicine
Department of Molecular Medicine and Metabolism
Department of Molecular Pharmacology
Department of Molecular Cell Biology
Department of Molecular Neuroscience
Department of Cell Regulation
Department of Bio-informational Pharmacology
Department of Autonomic Physiology
Project Unit
Devision of Pathophysiology
Department of Neuropathology
Department of Pathological Biochemistry
Department of Virology
Department of Developmental and
Regenerative Biology
Department of Criminal Psychiatry
Department of Immunology
Department of Molecular Pathogenesis
Frontier Research Unit
Virus Research Unit
Project Research Unit
Devision of Medical Genomics
Department of Molecular Cytogenetics
Department of Molecular Genetics
Department of Molecular Epidemiology
Department of Biochemical Genetics
Department of Functional Genomics
Department of Epigenetics
Department of Bioinformatics
Frontier Research Unit
Redox Response Cell Biology
Project Research Unit
Division of Integrative Research
Pathogenetic Regulation
Biosystem Generation
Neurotraumatology
Advanced Technology Laboratory
Genome Laboratory
Cellular and Proteome Research Laboratory
Laboratory of Recombinant Animals
Animal Research Laboratory
Laboratory of Anatomy and Cell Function
Bioresource Labotatory
Bioinformation Laboratory
School of Biomedical Science
15
MRI 2005
Department of Medical Bioinformatics
Genome Diversity
Computational Biology
Genome Structure and Regulation
Department of Applied Structural Biology
Structural Biology
Organic and Medical Chemistry
Medical Chemistry
Department of Functional Biology
Gene Expression
Molecular Neuroscience
Immunology
Biosystem Modeling