| Project/Area Number |
24651058
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Risk sciences of radiation/Chemicals
|
|---|
| Research Institution | Tohoku University |
|---|
Principal Investigator |
HWANG GIWOOK 東北大学, 薬学研究科(研究院), 講師 (00344680)
|
|---|
| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
|---|
| Keywords | トキシコロジー / カドミウム / 小胞体ストレス / 小胞体関連蛋白質分解系 |
|---|
| Research Abstract |
The molecular mechanisms underlying cadmium induced ER stress are not clearly understood. The levels of ERAD substrate were significantly increased by cadmium treatment, and were also increased by proteasome inhibitor treatment. However, the accumulation of ERAD substrates by cadmium was hardly accepted in cells treated with MG132. When the ERAD system was inhibited, levels of ER stress markers such as BiP and CHOP were significantly increased. ER stress-inducing agents such as tunicamycin, thapsigargin and dithiothreitol did not affect the levels of ERAD substrates. We conclude that cadmium may induce ER stress by inhibition of the function of the ERAD system and repression of the degradation of misfolded protein.
|
