Department of Developmental Genetics
Department
| Professor |
Ken-ichi Yamamura yamamura（at mark）gpo.kumamoto-u.ac.jp |
|---|---|
| Associate Professor |
Yoshikazu Hirate arakimi(at mark)gpo.kumamoto-u.ac.jp |
Research themes
[Names and Summaries of Research Projects]
Our main theme is "in vivo analyses on the gene-environment interaction in mammalian development and disease development" by full use of genome and developmental engineering techniques. Detailed research projects are as follows.
- Genome engineering: We are applying "exchangeable gene targeting method using Cre/mutant lox system" to analyze new genome function by the use of ES cells derived from Japanese wild mouse, MSM/Ms.
- Proteome analysis: We developed comprehensive system for proteome analysis using iTRAQ, HPLC, nano-LC, and mass spectrometer. We are searching disease-related and organ-specific markers using liver, sperm or blood.
- Pathogenesis of caudal regression syndrome: We revealed that Danforth' short tail mouse was caused by downregulation of Cdx2 and its downstream target genes induced by ectopic expression of Ptf1a. Based on this finding, we are analyzing etiology and patho-physiology of human caudal regression syndrome.
- Study on humanized mice:
(1) Establishment and application of mouse with human liver: We plan to establish mice with human liver using human hepatocytes derived from iPS cells. We will apply these humanized mice for evaluation of safety of iPS-derived hepatocytes and for analysis of patho-physiology of human diseases that are caused by the mutant genes expressed in liver. (2) Molecular mechanisms of hepatogenesis: Liver function can be achieved by the presence of precise microscopic structure. We are analyzing molecular mechanisms for building such microscopic structure. (3) Citrin deficiency: We are analyzing the patho-physiology of neonatal intrahepatic cholestasis (NICCD) and adult-onset type II citrullinemia (CTLN2) that are caused by the mutation of Citrin gene using patient's DNA, mouse with human liver derived from Patient's iPS cells. (4) Familial amyloidotic polyneuropathy (FAP): We are using humanized mice carrying both human transthyretin and retinol biding protein genes to analyzed patho-physiology of disease development and to devise a new way of treatment.
