pubmed-article:10397808 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10397808 | lifeskim:mentions | umls-concept:C0001483 | lld:lifeskim |
pubmed-article:10397808 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:10397808 | lifeskim:mentions | umls-concept:C0010453 | lld:lifeskim |
pubmed-article:10397808 | lifeskim:mentions | umls-concept:C0026764 | lld:lifeskim |
pubmed-article:10397808 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:10397808 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
pubmed-article:10397808 | lifeskim:mentions | umls-concept:C0301630 | lld:lifeskim |
pubmed-article:10397808 | lifeskim:mentions | umls-concept:C1512045 | lld:lifeskim |
pubmed-article:10397808 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:10397808 | pubmed:dateCreated | 1999-8-3 | lld:pubmed |
pubmed-article:10397808 | pubmed:abstractText | It is now well documented that apoptosis represents the prevalent mode of death in lymphoid cultures and occurs spontaneously in late-exponential phase of batch cultures following nutrient exhaustion. In an attempt to enhance the cell survival of these cell lines, we have initially engineered nonproducing NS/0 myeloma cells with a vector expressing the adenoviral E1B-19K protein. NS/0 cells transfected with E1B-19K were found to be more resistant to apoptosis occurring in the late phase of batch culture and under stressful conditions such as cultivation in glutamine-free medium or following heat shock. In this study, we have characterised a number of NS/0 subclones constitutively expressing different levels of E1B-19K, as well as several subclones in which the expression of E1B-19K was regulated by a tetracycline-controllable gene switch. We have found that a threshold E1B-19K level was required in order to achieve protection against apoptosis. The extent of resistance against cell death induced by nutrient deprivation in glutamine-free medium and in the late phase of batch cultures correlated with the level of E1B-19K expression up to an optimal level where further increases in E1B-19K levels did not result in significant additional protection. To assess the effects of E1B-19K on antibody productivity, an apoptosis-resistant NS/0 clone was then transfected with a chimeric antibody construct. Despite their improved viability, the antibody productivity of E1B-19K clones in batch culture was not significantly improved. Moreover, while the use of E1B-19K considerably delayed cell death, cells eventually died by apoptosis. Surprisingly, E1B-19K had no beneficial effect on the efficiency of fusion of NS/0 myelomas and splenocytes for the generation of hybridoma cells. Furthermore, the resulting hybridomas, although expressing E1B-19K at levels comparable to the myeloma parent, were no longer resistant to apoptosis. This indicates that the ability of E1B-19K to prevent apoptosis is not only dose-dependent but also seems to be cell-type dependent. | lld:pubmed |
pubmed-article:10397808 | pubmed:language | eng | lld:pubmed |
pubmed-article:10397808 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10397808 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10397808 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10397808 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10397808 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10397808 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10397808 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10397808 | pubmed:month | Jun | lld:pubmed |
pubmed-article:10397808 | pubmed:issn | 0006-3592 | lld:pubmed |
pubmed-article:10397808 | pubmed:author | pubmed-author:JolicoeurPP | lld:pubmed |
pubmed-article:10397808 | pubmed:author | pubmed-author:MassieBB | lld:pubmed |
pubmed-article:10397808 | pubmed:author | pubmed-author:GervaisCC | lld:pubmed |
pubmed-article:10397808 | pubmed:author | pubmed-author:MosserD DDD | lld:pubmed |
pubmed-article:10397808 | pubmed:author | pubmed-author:MercilleSS | lld:pubmed |
pubmed-article:10397808 | pubmed:author | pubmed-author:PaquetteDD | lld:pubmed |
pubmed-article:10397808 | pubmed:copyrightInfo | Copyright 1999 John Wiley & Sons, Inc. | lld:pubmed |
pubmed-article:10397808 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10397808 | pubmed:day | 5 | lld:pubmed |
pubmed-article:10397808 | pubmed:volume | 63 | lld:pubmed |
pubmed-article:10397808 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10397808 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10397808 | pubmed:pagination | 516-28 | lld:pubmed |
pubmed-article:10397808 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:10397808 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:10397808 | pubmed:articleTitle | Dose-dependent reduction of apoptosis in nutrient-limited cultures of NS/0 myeloma cells transfected with the E1B-19K adenoviral gene. | lld:pubmed |
pubmed-article:10397808 | pubmed:affiliation | Groupe d'Ingénierie des Cellules Animales, Institut de Recherche en Biotechnologie, Conseil National de Recherches du Canada, 6100 Avenue Royalmount, Montréal, PQ, Canada, H4P 2R2. | lld:pubmed |
pubmed-article:10397808 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10397808 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10397808 | lld:pubmed |