{"id":{"repo_id":"ajou","oai_identifier":"oai:repository.ajou.ac.kr:201003/7532"},"canonical_url":"https://search.dev.ndltd.org/etd/ajou/oai:repository.ajou.ac.kr:201003/7532","repository":{"repo_id":"ajou","name":"Ajou University","base_url":"http://repository.ajou.ac.kr/oai/request"},"display":{"title":"Regulation of mRNA expression through 3’ UTR sequences of IL6 gene in amino acid-deprived HeLa cells","abstract":"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.","abstract_html":"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.","abstract_has_math":false,"creators":["강, 정희"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["최, 용준","대학원 의생명과학과","201024346"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2012,"date_issued":"2012-10-25T05:14:06Z","date_published":"2012-10-25T05:14:06Z","updated_at":"2026-07-24T00:51:39Z","subjects":[],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000012350","000000012350"],"render_values":[{"text":"http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000012350","href":"http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000012350","code":true},{"text":"000000012350","href":null,"code":true}]}]},"links":{"outbound_url":"http://repository.ajou.ac.kr/handle/201003/7532","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["최, 용준","대학원 의생명과학과","201024346","강, 정희"]},{"key":"dc:creator","label":"Author","values":["강, 정희"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2012-10-25T05:14:06Z","2012"]},{"key":"dc:type","label":"Dc Type","values":["Thesis","Theses"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://repository.ajou.ac.kr/handle/201003/7532","http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000012350","000000012350"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["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.","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 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","Master"]},{"key":"dc:title","label":"Title","values":["Regulation of mRNA expression through 3’ UTR sequences of IL6 gene in amino acid-deprived HeLa cells","HeLa 세포주의 아미노산 결핍에서 IL6 유전자의 3’ UTR이 mRNA의 표현에 미치는 영향분석"]}]}],"canonical_facts":{"dc:contributor":["최, 용준","대학원 의생명과학과","201024346","강, 정희"],"dc:creator":["강, 정희"],"dc:date":["2012-10-25T05:14:06Z","2012"],"dc:description":["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.","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 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","Master"],"dc:identifier":["http://repository.ajou.ac.kr/handle/201003/7532","http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000012350","000000012350"],"dc:language":["en"],"dc:title":["Regulation of mRNA expression through 3’ UTR sequences of IL6 gene in amino acid-deprived HeLa cells","HeLa 세포주의 아미노산 결핍에서 IL6 유전자의 3’ UTR이 mRNA의 표현에 미치는 영향분석"],"dc:type":["Thesis","Theses"]},"updated_at":"2026-07-24T00:51:39Z"}