| Project/Area Number |
07671183
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Hematology
|
|---|
| Research Institution | TOKYO MEDICAL AND DENTAL UNIVERSITY |
|---|
Principal Investigator |
TAKASE Kozo TOKYO MEDICAL AND DENTAL UNIVERSITY,M.D., Ph.D., 医学部, 助手 (90211333)
|
|---|
| Project Period (FY) |
1995 – 1996
|
| Project Status |
Completed (Fiscal Year 1996)
|
| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥1,500,000 (Direct Cost: ¥1,500,000)
|
|---|
| Keywords | CDK inhibitor / cyclin E / NAD / DMSO |
|---|
| Research Abstract |
We investigated the relationship between the cell cycle status and the regulation of cyclin E expression on DMSO-arrested Raji cells. In arrested Raji Cells, abundant cyclin E and a detectable amount of cdk2 are observed in contrast to normal resting T cells where a small amount of cdk2 and an undetectable amount of cyclin E present. The enzyme activity of cyclin E or cdk2 in Raji cells is not demonstrated until just before the cell cycle recovery from DMSO-induced arrest, in regardless to the abundance of these components of the enzyme. As for the stimulation induced proliferation of normal T cells, the enzyme activity of cyclin E or cdk2 arises in a time course manner parallel to the appearance of cyclin E protein. Along this process, any known inhibitor against cdk is not detected as an obvious band in Western blotting. These indicate that the regulatory mechanisms of cyclin E/cdk2 activity in normal T cells and cell lines are quite different, and that the dysregulation of cell cycle progression in cell line is not supposed to be attributed by a deficiency of cdk inhibitor. In addition, we demonstrated an accumulation and a rapid consumption of NAD^+ across the cell cycle recovery from DMSO-arrest in Raji cells. We assume an activation of poly (ADP-ribose) polymerase plays an important role in this phenomenon where the amount of AMP is observed to increase in a reciprocal manner to the decrease in NAD^+.
|
