| Project/Area Number |
16K18538
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cell biology
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | タンパク質分解 / 糖鎖 / 小胞体 / 構造異常タンパク質 / 小胞体関連分解 / mannose trimming / EDEM |
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| Outline of Final Research Achievements |
ER-associated degradation (ERAD) is composed of glycoprotein and non-glycoprotein degradation pathways. By inhibition of glycoprotein degradation pathway, native but unstable or somewhat unfolded glycoproteins were stabilized, but degradation of severely misfolded glycoproteins was delayed only at early chase periods, but they were eventually degraded as in wild-type cells. We analyzed these molecular mechanisms.
We tried to knocked out the candidate gene, which target substrates from glycoprotein degradation pathway to non-glycoprotein degradation pathway, and found that the gene is essential for cells, indicating its importance. Using PITCh method, its low expression strains were established. The mutant strain includes some mutations in genomic level. We found that the strain is defective to degrade severely misfolded non-glycoproteins.
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