| Project/Area Number |
09044303
|
|---|
| Research Category |
Grant-in-Aid for international Scientific Research
|
| Allocation Type | Single-year Grants |
|---|
| Section | Joint Research |
|---|
| Research Field |
Molecular biology
|
|---|
| Research Institution | Osaka University |
|---|
Principal Investigator |
TSUJIMONOTO Yoshihide Osaka University Medical School, Professor, 医学部, 教授 (70132735)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
LAZEBNIK Yuri Cold Spring Harbor Laboratory, senior Staff Investigator, 研究員
SHIMIZU Shigeomi Osaka University Medidal School, Research Assistant, 医学部, 助手 (70271020)
KAMADA Shinji Osaka University Medidal School, Research Assistant, 医学部, 助手 (20243214)
EGUCHI Yutaka Osaka University Medical School, Associate Professor, 医学部, 助教授 (20243206)
|
|---|
| Project Period (FY) |
1997
|
| Project Status |
Completed (Fiscal Year 1997)
|
| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥2,200,000 (Direct Cost: ¥2,200,000)
|
|---|
| Keywords | apoptosis / mitochondria / bcl-2 / caspase |
|---|
| Research Abstract |
Apoptosis is an important suicide mechanism involved in a variety of biological phenomena including morphogenesis and homeostasis. Although apoptosis is an important theme not only in basic biology but also in medical field because dysregulation of apoptosis leads to various diseases such as cancer and Alzheimer's disease, the molecular basis of apoptosis is still largely unknown.
To study functions of known genes involved in apoptosis and also to identify new apoptosis-related genes, in vitro apoptosis system would be extremely useful. Although one system originally developed by Y.Lazebnik has been widely used, we have developed a new system which mimics better in vivo apoptosis than Lazebnik's, and identified several components that are responsible for apoptotic morphology of the nucleus. Previously we showed that mitochondrial membrane potential loss which is inhibited by Bcl-2, plays an important role in apoptosis. To analyze the biochemical basis of Bcl-2 anti-apoptotic function, we have established a system with isolated mitochondria in which Bcl-2 functions to prevent membrane potential loss, and elucidated that Bcl-2 prevents membrane potential loss by enhancing proton efflux.
These systems would be very useful for study of molecular basis of apoptosis, and likely provide new insights into control of diseases develeping though deregulation of apoptosis.
|
