DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Jae-Seong | ko |
dc.contributor.author | Ha, Tae-Kwang | ko |
dc.contributor.author | Park, Jin-Hyoung | ko |
dc.contributor.author | Lee, Gyun-Min | ko |
dc.date.accessioned | 2013-08-14T01:26:35Z | - |
dc.date.available | 2013-08-14T01:26:35Z | - |
dc.date.created | 2013-07-18 | - |
dc.date.created | 2013-07-18 | - |
dc.date.issued | 2013-08 | - |
dc.identifier.citation | BIOTECHNOLOGY AND BIOENGINEERING, v.110, no.8, pp.2195 - 2207 | - |
dc.identifier.issn | 0006-3592 | - |
dc.identifier.uri | http://hdl.handle.net/10203/175061 | - |
dc.description.abstract | Genetic engineering approaches to inhibit cell death in Chinese hamster ovary (CHO) cell cultures have been limited primarily to anti-apoptosis engineering. Recently, autophagy has received attention as a new anti-cell death engineering target in addition to apoptosis. In order to achieve a more efficient protection of cells from the stressful culture conditions, the simultaneous targeting of anti-apoptosis and pro-autophagy in CHO cells (DG44) was attempted by co-overexpressing an anti-apoptotic protein, Bcl-2, and a key regulator of autophagy pathway, Beclin-1, respectively. Co-overexpression of Bcl-2 and Beclin-1 exhibited a longer culture period as well as higher viability during serum-free suspension culture, compared with the control (without co-overexpression of Bcl-2 and Beclin-1) and Bcl-2 overexpression only. In addition to the efficient inhibition of apoptosis by Bcl-2 overexpression, Beclin-1 overexpression successfully induced the increase in the autophagic marker protein, LC3-II, and autophagosome formation with the decrease in mTOR activity. Co-immunoprecipitation and qRT-PCR experiments revealed that the enforced expression of Beclin-1 increased Ulk1 expression and level of free-Beclin-1 that did not bind to the Bcl-2 despite the Bcl-2 overexpression. Under other stressful culture conditions such as treatment with sodium butyrate and hyperosmolality, co-overexpression of Bcl-2 and Beclin-1 also protected the cells from cell death more efficiently than Bcl-2 overexpression only, implying the potential of autophagy induction. Taken together, the data obtained here provide the evidence that pro-autophagy engineering together with anti-apoptosis engineering yields a synergistic effect and successfully enhances the anti-cell death engineering of CHO cells. Biotechnol. Bioeng. 2013; 110: 2195-2207. (c) 2013 Wiley Periodicals, Inc. | - |
dc.language | English | - |
dc.publisher | WILEY-BLACKWELL | - |
dc.subject | HAMSTER OVARY CELLS | - |
dc.subject | REGULATES AUTOPHAGY | - |
dc.subject | SODIUM-BUTYRATE | - |
dc.subject | CULTURE | - |
dc.subject | PATHWAY | - |
dc.subject | GENES | - |
dc.subject | BATCH | - |
dc.subject | MACROAUTOPHAGY | - |
dc.subject | METABOLISM | - |
dc.subject | EXPRESSION | - |
dc.title | Anti-cell death engineering of CHO cells: Co-overexpression of Bcl-2 for apoptosis inhibition, Beclin-1 for autophagy induction | - |
dc.type | Article | - |
dc.identifier.wosid | 000320930800014 | - |
dc.identifier.scopusid | 2-s2.0-84879605428 | - |
dc.type.rims | ART | - |
dc.citation.volume | 110 | - |
dc.citation.issue | 8 | - |
dc.citation.beginningpage | 2195 | - |
dc.citation.endingpage | 2207 | - |
dc.citation.publicationname | BIOTECHNOLOGY AND BIOENGINEERING | - |
dc.identifier.doi | 10.1002/bit.24879 | - |
dc.contributor.localauthor | Lee, Gyun-Min | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | Bcl-2 | - |
dc.subject.keywordAuthor | Beclin-1 | - |
dc.subject.keywordAuthor | CHO-DG44 | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | autophagy | - |
dc.subject.keywordPlus | HAMSTER OVARY CELLS | - |
dc.subject.keywordPlus | REGULATES AUTOPHAGY | - |
dc.subject.keywordPlus | SODIUM-BUTYRATE | - |
dc.subject.keywordPlus | CULTURE | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | GENES | - |
dc.subject.keywordPlus | BATCH | - |
dc.subject.keywordPlus | MACROAUTOPHAGY | - |
dc.subject.keywordPlus | METABOLISM | - |
dc.subject.keywordPlus | EXPRESSION | - |
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