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MARCH5에 의한 RIG-I/MAVS 신호전달의 조절
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.advisor | 조혜성 | - |
| dc.contributor.author | 김성광 | - |
| dc.date.accessioned | 2019-04-01T16:40:51Z | - |
| dc.date.available | 2019-04-01T16:40:51Z | - |
| dc.date.issued | 2019-02 | - |
| dc.identifier.other | 28661 | - |
| dc.identifier.uri | https://dspace.ajou.ac.kr/handle/2018.oak/14959 | - |
| dc.description | 학위논문(석사)--아주대학교 일반대학원 :의생명과학과,2019. 2 | - |
| dc.description.tableofcontents | I. INTRODUCTION 1 II. MATERIALS AND METHODS 4 1. Plasmids and antibodies 4 2. Cell culture 4 3. Western blot analysis 5 4. Transfection of DNAs and siRNA 6 5. MAVS aggregate - insoluble fraction 6 6. Generation of MARCH5 conditional knock-out mouse. 7 III. RESULTS 9 1. RIG-I oligomer and MAVS aggregate increase upon poly(I:C) transfection 9 2. Increase of insoluble RIG-I oligomer after viral condition 12 3. The levels of IFN-beta and IL-6 increase in MARCH5 knock-out mouse upon virus challenge 14 4. MARCH5 negatively regulates oligomeric RIG-I 19 5. MARCH5 directly binds to RIG-I protein 23 6. RIG-I/MAVS complex formation is important for interaction with MARCH5 25 IV. DISCUSSION 27 V. REFERENCES 30 국문요약 36 | - |
| dc.language.iso | eng | - |
| dc.publisher | The Graduate School, Ajou University | - |
| dc.rights | 아주대학교 논문은 저작권에 의해 보호받습니다. | - |
| dc.title | MARCH5에 의한 RIG-I/MAVS 신호전달의 조절 | - |
| dc.title.alternative | Seong-Gwang Kim | - |
| dc.type | Thesis | - |
| dc.contributor.affiliation | 아주대학교 일반대학원 | - |
| dc.contributor.alternativeName | Seong-Gwang Kim | - |
| dc.contributor.department | 일반대학원 의생명과학과 | - |
| dc.date.awarded | 2019. 2 | - |
| dc.description.degree | Master | - |
| dc.identifier.localId | 905275 | - |
| dc.identifier.uci | I804:41038-000000028661 | - |
| dc.identifier.url | http://dcoll.ajou.ac.kr:9080/dcollection/common/orgView/000000028661 | - |
| dc.description.alternativeAbstract | The innate immune system has an important role in the mammalian immune response. Recent study has demonstrated that mitochondria take part in a broad range of innate immune pathways, functioning as signal platforms and resulting in activation of immune responses. Previously, our lab found that MARCH5 regulates immune response by resolving MAVS prion-like aggregates during viral infection. The present study revealed the kinetics of RIG-I/MAVS oligomerization upon poly(I:C) transfection. RIG-I and MAVS began to form oligomer, respectively after 12 hrs of poly(I:C) transfection. This was accompanied with accumulation of RIG-I and MAVS protein levels. At 36hrs after stimulation, the oligomerized RIG-I and MAVS proteins were accumulated in the NP_40-insoluble fractions, suggesting that the RIG-I/MAVS oligomers form a strong insoluble protein aggregates in cells. I found that MARCH5 not only targeted the oligomerized MAVS protein but also caused a significant reduction of the oligomerized RIG-I levels, of which degradation is mediated through a proteasome-dependent manner. In bone-marrow derived macrophage cell (BMDM) from MARCH5 knockout mice secreted high amount of type-I interferon secretion in response to poly(I:C) transfection. Approach to oligomeric complex provides understanding of relationship between RIG-I/MAVS oligomers and MARCH5. That make the reason I proposed that RIG-I and MAVS oligomers can be dual-targeted by MARCH5 during innate immune response. | - |
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- Graduate School of Ajou University > Department of Biomedical Sciences > 3. Theses(Master)
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