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HeLa 세포주의 아미노산 결핍에서 IL6 유전자의 3’ UTR이 mRNA의 표현에 미치는 영향분석
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.advisor | 최 용준 | - |
| dc.contributor.author | Jung Hee Kang | - |
| dc.date.accessioned | 2019-10-21T07:17:18Z | - |
| dc.date.available | 2019-10-21T07:17:18Z | - |
| dc.date.issued | 2012-02 | - |
| dc.identifier.other | 12350 | - |
| dc.identifier.uri | https://dspace.ajou.ac.kr/handle/2018.oak/17815 | - |
| dc.description | 학위논문(석사)아주대학교 일반대학원 :의생명학과,2012. 2 | - |
| dc.description.tableofcontents | ABSTRACT ⅰ TABLE OF CONTENTS ⅱ LIST OF FIGURES ⅳ LIST OF TABLES ⅴ ABBREVIATION ⅴ Ⅰ. INTRODUCTION 1 Ⅱ. MATERIALS AND METHODS 3 A. Cell, antibodies and other reagents 3 B. Expression constructs and lentiviral transfections 3 C. Real time RT PCR 4 D. Western blot 4 Ⅲ. RESULTS 6 A. IL6 induction in amino acid-deprived HeLa cell 6 B. Constructions of GFP-reporter plasmids containing 3’UTR of IL6 mRNA 6 C. Effects of 3’UTR on induction of IL6 reporter in amino acids-deprived HeLa cells 8 D. Effect of partial 3’UTR on induction of IL6 reporter in amino acids-deprived HeLa cell 8 E.GFP expressions in HeLa cells infected with pCMV or pCMV-UTR before/after amino acid deprivation 8 F. Effects of STAT3 and NF-kB transcriptional factors on IL6 3’UTR in IL6 induction of amino acid deprived HeLa cells 14 G. Effects of MAP kinase inhibitor on IL6 3’ UTR in amino acids-deprived HeLa cells 14 Ⅳ. DISCUSSION 19 Ⅴ. CONCLUSION 21 REFERENCES 22 국문요약 26 | - |
| dc.language.iso | eng | - |
| dc.publisher | The Graduate School, Ajou University | - |
| dc.rights | 아주대학교 논문은 저작권에 의해 보호받습니다. | - |
| dc.title | HeLa 세포주의 아미노산 결핍에서 IL6 유전자의 3’ UTR이 mRNA의 표현에 미치는 영향분석 | - |
| dc.title.alternative | Kang Jung Hee | - |
| dc.type | Thesis | - |
| dc.contributor.affiliation | 아주대학교 일반대학원 | - |
| dc.contributor.alternativeName | Kang Jung Hee | - |
| dc.contributor.department | 일반대학원 의생명과학과 | - |
| dc.date.awarded | 2012. 2 | - |
| dc.description.degree | Master | - |
| dc.identifier.localId | 570028 | - |
| dc.identifier.url | http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000012350 | - |
| dc.description.alternativeAbstract | ER stress responses and autophagic responses triggered by amino acid-deprivation of cancer cells activate STAT3 and NF-κB transcriptional factors subsequently to induce IL6 cytokines. Here, it was investigated whether 3’UTR of IL6 mRNA played a role in IL6 induction through cellular stress responses. In the studies with GFP-reporter containing 3’UTR of IL6 mRNA, it was elucidated that 3’UTR contributed to increase of IL6 mRNA after amino acid-starvation, and its motifs seemed to be broadly distributed according to deletion mutants studies of IL6 3’UTR. NF-κB functioned in 3’UTR to partially contribute to stabilization of IL6 mRNA according to knock-down experiments of p65, NF-κB subunit. Finally, treatments of p38 MAP kinase inhibitor, SB203580 markedly blocked mRNA stabilization through 3’UTR as well as IL6 induction after amino acid-starvation, suggesting that p38-MK2/3-TTP pathway is evidently activated and implicated in stabilization of IL6 mRNA during starvation of cancer cells. Conclusively, these studies indicate that stress signals via NF-κB and p38 lead to mRNA stabilization through 3’UTR sequences, and their molecular mechanism would need to be further studied. | - |
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