| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Research Abstract |
I investigated the molecular mechanism of regulation of TASK1 channels in endocrine cells. Pharmacological and molecular biological analyses showed that TASK1 channels are regulated by the clathrin-dependent endocytosis in NGF-stimulated adrenal medullary and PC12 cells. Mutation analysis of the TASK1 channel revealed that the dileucine motif was involved in at least part of the endocytosis. Furthermore, I showed that Src, PLC and PI3K are involved in NGF-induced endocytosis of TASK1 channels in PC12 cells. Additionally, the expression of TASK1 channels at the protein and mRNA levels was suppressed in PC12 cells treated with NGF for 2 weeks. These results indicate that NGF suppresses the expression of TASK1 channels in the plasma membrane via not only endocytosis but also the inhibition of gene transcription.
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