Tateki Kikuchi

Tateki Kikuchi

Emeritus Researcher of the National Institute of
Neuroscience, NCNP, Tokyo

Scientific Advisor for Pathology Core and Mouse Clinic Project

Personal Information:
Name in full: Tateki Kikuchi
Present address: 4 – 2 - 88, Takamori, Izumi-ku, Sendai 981-3203, Japan
Tel/fax: +81-22-378-0315
E-mail: kikuchi@ibms.sinica.edu.tw or tkikuchi@ma.mni.ne.jp

Specialized Field:
1. Animal Pathology and Anatomy
2. Molecular Genetics
3. Laboratory Animal Science


Name of University
Dates attended
Tohoku University
Sendai, Japan



Tohoku University
Graduate course
For Master degree




Tohoku University
Sendai, Japan


Professional Experience:

1967 – 1984

Tohoku University, Department of Animal Science, Sendai, Japan


Postdoctoral Fellow
Supported by Muscular Dystrophy Association of America.University of California-Davis, Department of Animal Science, Davis, CA, USA


Visiting Research Fellow
Supported by Deutsche Forshunngsgemeinshaft (DFG), Universität des Saarlandes, Physiologishes Institüt, Homburg, Saar, Germany


Associate Professor
Tohoku University, Department of Animal Science, Sendai, Japan


Department of Animal Models for Human Disease, National Institute of Neuroscience, NCNP, Kodaira, Tokyo, Japan


Honorary scientist
National Institute of Neuroscience, NCNP, Kodaira, Tokyo,Japan


Visiting Professor
Miyagi University, Sendai, Japan


Visiting Research Fellow
Institute of Biomedical Science, Academia Sinica, Taipei,Taiwan

Research Description:

      Post-genome project is under way worldwide using mice carrying spontaneous, induced, and genetically engineered mutations, which allow us to apply efficient phenotype-based surveys of gene function, and to define genes associated to human diseases. A chemical N-ethyl-N- nitrosourea (ENU) that induces point mutations at a high rate provided a vital tool to generate new mouse models to determining gene function on a mouse chromosome, which we can extrapolate to predict function on a human chromosome. Up to date, the ENU program in the IBMS already related several potential mutant phenotypes to human diseases, such as Maple syrup urine disease, lipotoxic cardiomyopathy, and cardiovascular ATS that is underway.
      Among animals, mice will play a major role to understanding mammalian genetic systems, since they are small in body size, short in life span with high fertility, and carry closely related set of genes to humans. To accomplish the determination of the relationship between genetic variation and phenotype, a number of mice must be screened for behavioral and blood based parameters, and pathological evaluation will be an important component to characterize mutant phenotypes more precisely.
      The Mouse Clinic Project was founded May 2008 at the IBMS to give efficient phenotype-driven approach to studying on gene function and mouse models for human diseases. Once mice with aberrant phenotypes identified in our screens, all database will be posted regularly on our website and will be made available broadly to scientists with interests.

Research Description:

  1. Suh JG, Ichihara N, Saigoh K, Nakabayashi O, Yamanishi T, Tanaka K, Wada K, Kikuchi T: An in-frame deletion in peripheral myelin protein-22 gene causes hypomyelination and cell death of the Schwann cells in the new Trembler mutant mice. Neuroscience. 1997,79, 735-744.
  2. Kunita R, Nakabayashi O, Wu JY, Hagiwara Y, Mizutani M, Pennybacker M, Chen YT, Kikuchi T: Molecular cloning of acid alpha-glucosidase cDNA of Japanese quail (Coturnix coturnix japonica) and the lack of its mRNA in acid maltase deficient quails.
    Biochim Biophys Acta. 1997, 1362, 269-278.
  3. Kikuchi T, Yang HW, Pennybacker M,Ichihara N, Mizutani M, Van Hove JL, Chen YT: Clinical and metabolic correction of pompe disease by enzyme therapy in acid maltase-deficient quail. J Clin Invest. 1998, 101, 827-833.
  4. Saigoh K, Wang YL, Suh JG, Yamanishi T, Sakai Y, Kiyosawa H, Harada T, Ichihara N, Wakana S, Kikuchi T, Wada K: Intragenic deletion in the gene encoding ubiquitin carboxy-terminal hydrolase in gad mice. Nat Genet. 1999, 23, 47-51.
  5. Kurihara LJ, Kikuchi T, Wada K, Tilghman SM: Loss of Uch-L1 and Uch-L3 leads to neurodegeneration, posterior paralysis and dysphagia. Hum Mol Genet. 2001, 10:1963-1970.
  6. Ando Y, Ichihara N, Takeshita S, Saito Y, Kikuchi T, Wakasugi N: Histological and ultrastructural features in the early stage of Purkinje cell degeneration in the cerebellar calcification (CC) rat. Exp Anim. 2004, 53, 81-88.
  7. Matsushima Y, Kikuchi T, Kikuchi H, Ichihara N, Ishikawa A, Ishijima Y, Tachibana M: A new mouse model for infantile neuroaxonal dystrophy, inad mouse, maps to mouse chromosome 1. Mamm Genome. 2005, 16:73-78.
  8. Nakabayashi O, Setsuie R, Sekine M, Kunita R, Mizutani M, Kikuchi T: A single base-pair deletion in exon 7 in qgaa1 gene responsible for acid maltase deficiency in Japanese quail (Coturnix Coturnix Japonica). Basic Appl Myol. 2005, 15: 19-21.
  9. Kao HJ, Cheng CF, Chen YH, Hung SI, Huang CC, Millington D, Kikuchi T, Wu JY, Chen YT: ENU mutagenesis identifies mice with cardiac fibrosis and hepatic steatosis caused by a mutation in the mitochondrial trifunctional protein beta-subunit.. Hum Mol Genet. 2006, 15, 3569-3577.
  10. Matsumoto H, Maruse H, Inaba Y, Yoshizawa K, Sasazaki S, Fujiwara A, Nishibori M, Nakamura A, Takeda S, Ichihara N, Kikuchi T, Mukai F, Mannen H: The ubiquitin ligase gene (WWP1) is responsible for the chicken muscular dystrophy. FEBS Lett. 2008, 582: 2212-2218.