| Project/Area Number |
24870025
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Cell biology
|
|---|
| Research Institution | Tokyo Women's Medical University |
|---|
Principal Investigator |
FUJIKI Kota 東京女子医科大学, 医学部, 助教 (80632504)
|
|---|
| Project Period (FY) |
2012-08-31 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | 重金属 / ストレス応答 / シグナル伝達 / 重金属ストレス / MAPK経路 / セロトニン / 線虫 / 分子生物学 |
|---|
| Research Abstract |
Heavy metals are important environmental pollutants and have been known to induce various damages in vivo and in vitro through the different mechanisms including the overproduction of reactive oxygen species. Organisms might have the environmental stress adaptation mechanisms (stress sensing, signaling, and response) for the survival against the exposure to heavy metals. In the present study, we examined the molecular mechanisms responsible for the stress adaptation following exposure to copper and cadmium. We found that the neuronal transmitter serotonin functions as a copper stress sensor in Caenorhabditis elegans. We also revealed that PI3K/Akt signaling pathway plays a role in the cell survival via regulation of expression or activity of some transcription factors including FOXO3a and ATF4 in human renal proximal tubular cells exposed to cadmium.
|
