Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, Tsung-Yih | en_US |
dc.contributor.author | Lin, Hsiao-Hsien | en_US |
dc.contributor.author | Chen, Chien-Lung | en_US |
dc.contributor.author | Hwang, Shiaw-Min | en_US |
dc.contributor.author | Tseng, Ching-Ping | en_US |
dc.date.accessioned | 2015-07-21T08:28:27Z | - |
dc.date.available | 2015-07-21T08:28:27Z | - |
dc.date.issued | 2015-01-02 | en_US |
dc.identifier.issn | 0732-8303 | en_US |
dc.identifier.uri | http://dx.doi.org/10.1080/07328303.2014.977908 | en_US |
dc.identifier.uri | http://hdl.handle.net/11536/124385 | - |
dc.description.abstract | In this study, we found the specific growth rate of CHO cells being reduced when glucose increased from 1 to 10g/L. Under high glucose, we show a 41% increase in lactate dehydrogenase activity consistent with a 70% rate increase in lactate production. The pyruvate kinase activity was significantly increased. However, the activities of citrate synthase, isocitrate dehydrogenase, and malate dehydrogenase involved in the TCA cycle were attenuated. We propose that pyruvate produced from glycolysis is utilized in a lesser extent over the TCA cycle under high-glucose conditions. Thus, the pyruvate is largely converted to lactate, which is toxic to the cells. | en_US |
dc.language.iso | en_US | en_US |
dc.subject | Glucose and TCA cycle enzymes | en_US |
dc.subject | Growth rate | en_US |
dc.subject | ICDH | en_US |
dc.subject | Glucose flux in glycolysis | en_US |
dc.subject | CHO cells | en_US |
dc.title | Inhibitory Effect of Excessive Glucose on Its Biochemical Pathway and the Growth of Chinese Hamster Ovary (CHO) Cells | en_US |
dc.type | Article | en_US |
dc.identifier.doi | 10.1080/07328303.2014.977908 | en_US |
dc.identifier.journal | JOURNAL OF CARBOHYDRATE CHEMISTRY | en_US |
dc.citation.volume | 34 | en_US |
dc.citation.epage | 11 | en_US |
dc.contributor.department | 生物科技學系 | zh_TW |
dc.contributor.department | Department of Biological Science and Technology | en_US |
dc.identifier.wosnumber | WOS:000349119200001 | en_US |
dc.citation.woscount | 0 | en_US |
Appears in Collections: | Articles |