| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Research Abstract |
Pin1 was degraded in severe damaged liver, therefore, regeneration was suppressed through decreased activation of NF-kappaB. In contrast, Pin1 expression was maintained in mild damaged liver. Therefore, Pin1 bound to NF-kappaB-p65 and generated Pin1-NF-kappaB-p65 complex. This complex activated NF-kappaB and induced liver regeneration. Moreover, cell proliferation was inhibited in severe damaged hepatocyte induced by H2O2 stimulation in vitro, through decreased expression of Pin1 and Pin1-NF-kappaB-p65 complex and decreased activation of NF-kappaB. In conclusion, Pin1 is an important endogenous regulator of liver regeneration in severe damaged liver,and is a potential therapeutic target for liver failure after extended hepatectomy.
|
