Zobrazeno 1 - 10
of 23
pro vyhledávání: '"Yong J. Lee"'
Autor:
Dae Hee Lee, Yong J. Lee
Publikováno v:
Journal of Cellular Biochemistry. 105:546-553
Quercetin, a ubiquitous bioactive plant flavonoid, has been shown to inhibit the proliferation of cancer cells and induce the accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha) in normoxia. In this study, under hypoxic conditions (1% O(2)),
Thermotolerance expression in mitotic CHO cells without increased translation of heat shock proteins
Autor:
Michael J. Borrelli, Diane M. Stafford, Peter M. Corry, Yong J. Lee, Lisa A. Karczewski, Cynthia M. Rausch
Publikováno v:
Journal of Cellular Physiology. 169:420-428
The objective of this study was to unequivocally demonstrate thermotolerance expression in mammalian cells in the absence of stress-induced synthesis of heat shock proteins (HSPs). Mitotic cells were selected as an experimental system since their gen
Publikováno v:
Journal of Thermal Biology. 17:305-312
1. 1.|The temperature-sensitive mutant CHO-tsH1 and wild type (CHO-SC) cells became thermal resistant when cells were treated for either 2 h at 39.5°C before heating at 43°C or 2 h with 10 μg/ml cycloheximide (CHM) before and during heating at 43
Publikováno v:
Journal of Thermal Biology. 17:313-316
1. 1.|We investigated the mechanism of cycloheximide-induced heat protection. We proposed a hypothesis to account for the mechanism [Lee and Dewey (1986) Radiat. Res.106, 98–110]. 2. 2.|Cycloheximide protects cells from hyperthermic killing by mean
Publikováno v:
Journal of Thermal Biology. 17:241-249
1. 1.|When L929 cells were treated with 10 μg/ml cycloheximide, 100 μg/ml puromycin, or 50 mM histidinol 2 h before and during heating at 43°C, these drugs afforded heat protection, i.e. an 8-fold increase in survival from 6 × 10−2 to 4.5 × 10
Publikováno v:
Journal of Cellular Physiology. 149:396-402
The mechanism of histidinol (HST)-induced heat protection was investigated to test the hypothesis that the cessation of protein synthesis itself is one of the events involved in heat protection. For this study, we isolated three HST-resistant mutant
Publikováno v:
Journal of Cellular Physiology. 149:202-207
We investigated whether or not a 50 kDa glycoprotein might play an important role in protein synthesis-independent thermotolerance development in CHO cells. When cells were heated for 10 min at 45.5 degrees C, they became thermotolerant to a heat tre
Publikováno v:
Biochemical and Biophysical Research Communications. 177:575-581
Protein denaturation resulting from temperatures between 42.0 degrees C and 50 degrees C has been observed and implicated as the lethal lesion for hyperthermic cell killing. A logical corollary is that protection against hyperthermic killing requires
Publikováno v:
Journal of Cellular Physiology. 144:401-407
The possible mechanism for heat protection by the protein synthesis inhibitor histidinol was investigated in CHO cells. Histidinol (HST, 5 mM), an analogue of the essential amino acid L-histidine, added for 2 hr before and during heating at 43 degree
Publikováno v:
International Journal of Hyperthermia. 6:591-595
To investigate the possibility that heat-induced protein degradation may play a role in heat killing of mammalian cells, we have compared cellular survival and protein degradation rates for cells treated with cycloheximide, puromycin, or histidinol.