Abstract

Abstract Shocked cells have been examined with respect to their sensitivity to inhibitors of active transport. They behave similarly to unshocked cells except that their transport ability is reduced. The process of restoration of active transport has been studied. Metabolic energy appears to be necessary to restore the uptake ability of shocked cells. Evidence is presented which suggests that the galactose- and leucine-binding proteins can become reassociated with the shocked cells. The process shows saturation kinetics and results in an increase in transport ability. We speculate that there are specific sites capable of interacting with the binding proteins. In addition to binding protein, another nondialyzable factor in shock fluid is found to be active in restoration of transport. This factor is precipitated by low concentrations of ammonium sulfate and does not have binding properties. Its activity is substantial and restoration of transport to nearly the original level can be shown only when this factor is used in combination with binding protein.

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