| Project/Area Number |
18580092
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Applied biochemistry
|
|---|
| Research Institution | Kyoto Institute of Technology |
|---|
Principal Investigator |
IKURA Koji Kyoto Institute of Technology, Graduate Schoolof Seicnce and Technology, Professor (00101246)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
ICHIKAWA Akira Kyoto Institute of Technology, Graduate School of Science and Technology, Assistant Professor (90346122)
|
|---|
| Project Period (FY) |
2006 – 2007
|
| Project Status |
Completed (Fiscal Year 2007)
|
| Budget Amount *help |
¥3,920,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥420,000)
Fiscal Year 2007: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2006: ¥2,100,000 (Direct Cost: ¥2,100,000)
|
|---|
| Keywords | bio-cross-linking enzyme / protein cross-linking enzyme / transglutaminase / transglutaminase substrate / transglutaminase function / ショウジョウバエ |
|---|
| Research Abstract |
This research project was carried out to analyze the physiological functions of protein cross-linking enzyme transglutaminase (TG). 1. In rat liver extract, arginase-I (AI) and fructose 1, 6-bisphosphatase (FBPase) were identified as new protein substrate candidates of TG. Activities of both enzymes decreased through the amine incorporation into these enzyme proteins by TG, suggesting the possibility of an involvement of TG in the regulation of glucose and arginine metabolisms. 2. Human brain proteins that interact with human brain TG(hbTG) were searched by use of yeast two-hybrid method. Low molecular weight G proteins Rin and Rit were identified as interacting protein candidates, but their interactions with hbTG were not confirmed by the pull-down assay. 3. Functional analysis of Drosophila TG (dTG) was performed. dTG gene seemed to be transcribed throughout all developmental stages. Knockdown of dTG in the whole body resulted in lethality at the late stage of pupa, indicating that dTG is essential for Drosophila development Over-expression of dTG at eye imaginal discs by GAL4-UAS targeted expression system caused rough eye phenotype. The induced rough eye phenotype is probably attributable to apoptosis caused through the activation of JNK signaling. Over-expression and knockdown of dTG at wing imaginal discs caused extra wing veins and blistered wings, respectively. These resulats indicated that the expression level of dTG in wing imaginal discs may affect the development of wing veins.
|
