Since there was a progressive transition of proliferating cells into a non-proliferating resting state, as well as an increased rate of cell loss in the aging ascites tumor, we examined whether cell loss preferentially affected the nonproliferating or the proliferating cells. The kinetics of cell lo
Phosphate transport in ehrlich ascites tumor cells and the effect of arsenate
β Scribed by Charles Levinson
- Publisher
- John Wiley and Sons
- Year
- 1972
- Tongue
- English
- Weight
- 401 KB
- Volume
- 79
- Category
- Article
- ISSN
- 0021-9541
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β¦ Synopsis
The effect of extracellular Pi and arsenate on Pi-transport in Ehrlich ascites tumor cells has been studied. Pi-transport can be described by Michaelis-Menten kinetics; the maximal flux equal to 44 mmoles (kg cell water)-' hour-' and K m equal to 3.3 X 1 0 -4 M. Arsenate is a competitive inhibitor of Pi-transport with an inhibition constant ( K i ) equal to 2.41 X M.
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A common feature of many tumors is an increase in glucose catabolism during tumor growth. We studied the mechanism of this phenomenon by using Ehrlich ascites tumor bearing mice as the animal model. We found that Ehrlich ascites tumor cells possess only glucose transporter 1 (GLUT1) and GLUT3 but no
## Abstract The total lipid content of whole cells and isolated nuclei of Ehrlich ascites tumors was found to increase in parallel with increasing age. Mainly triglycerides were accumulated both in the cells and in the nuclei, but the nuclear fraction showed also an increase in the total cholestero
## Ouabain induced inhibition of cation transport and cell division in Ehrlich mouse ascites tumor cells is reversible, suggesting that this agent does not bind irreversibly to its site of action.
## Abstract We have investigated the effects of La^+3^ binding to the surface of Ehrlich ascites tumor cells on cell electrophoretic mobility and passive movements of Na^+^ and K^+^. Incubation of tumor cells in La^+3^βcontaining media results in a La^+3^ concentrationβdependent decrease in net sur
## Abstract The way in which the lectins concanavalin A (Con A) and __Ricinus communis__ agglutinin (Ricin) alter the K^+^ content of Ehrlich ascites tumor cells was investigated. Unidirectional and net fluxes were determined in unwashed cells during a time course following lectin addition. Total i