Regulation of active alpha-aminoisobutyric acid transport expressed in membrane vesicles from mouse fibroblasts.

Publisher Website
Google Scholar
Abstract
Membrane vesicles isolated from untransformed Balb/c and Swiss mouse fibroblasts and those transformed by SV 40 catalyzed carrier-mediated uptake of L-.alpha.-aminoisobutyric acid. Concentrative uptake required the presence of a Na+ gradient (external Na+ > internal Na+) and occurred independently of endogenous (Na+ + K+)ATPase activity. This process is electrogenic, since uptake was stimulated by a K+ diffusion gradient (internal > external) in the presence of valinomycin or the addition of the Na+ salt of a permeant ion, conditions expected to create an interior negative membrane potential. The initial rate of concentrative uptake of L-.alpha.-aminoisobutyric acid and its maximal accumulation, driven by a standard Na+ gradient, were decreased in vesicles from density-inhibited, untransformed cells and increased in those from cells transformed by SV 40, compared with vesicles from proliferating untransformed cells. An increased maximal velocity (Vmax) of uptake stimulated by Na+ gradient was observed in vesicles from transformed cells compared with those from untransformed cells, suggesting an increase in the number of carriers or their mobility. Since the relative extent of accumulation of this model amino acid driven by a standard Na+ gradient also differed with growth or transformed status, an additional possibility for cellular regulation of this process could be alteration of membrane Na+ permeability or carrier response to Na+.