The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Influence of cloned voltage-gated K+ channel expression on alanine transport, Rb+ uptake, and cell volume.

Voltage-gated K+ channels are involved in regulation of action potential duration and in setting the resting membrane potential in nerve and muscle. To determine the effects of voltage-gated K+ channel expression on processes not associated with electrically excitable cells, we studied cell volume, membrane potential, Na(+)-K(+)-ATPase activity, and alanine transport after the stable expression of the Kv1.4 and Kv1.5 human K+ channels in Ltk- mouse fibroblasts (L-cells). The fast-activating noninactivating Kv1.5 channel, but not the rapidly inactivating Kv1.4 channel, prevented dexamethasone-induced increases in intracellular volume and inhibited Na(+)-K(+)-ATPase activity by 25%, as measured by 86Rb+ uptake. Alanine transport, measured separately by systems A and ASC, was lower in Kv1.5-expressing cells, indicating that the expression of this channel modified the Na(+)-dependent amino acid transport of both systems. Expression of the Kv1.4 channel did not alter alanine transport relative to wild-type or sham-transfected cells. The changes specific to Kv1.5 expression may be related to the resting membrane potential induced by this channel (-30 mV) in contrast to that measured in wild-type sham-transfected, or Kv1.4-transfected cells (-2 to 0 mV). Blocking of the Kv1.5 channel by 60 microM quinidine negated the effects of Kv1.5 expression on intracellular volume, Na(+)-K(+)-ATPase, and Na(+)-dependent alanine transport. These results indicate that delayed rectifier channels such as Kv1.5 can play a key role in the control of cell membrane potential, cell volume, Na(+)-K(+)-ATPase activity, and electrogenic alanine transport across the plasma membrane of electrically unexcitable cells.[1]


  1. Influence of cloned voltage-gated K+ channel expression on alanine transport, Rb+ uptake, and cell volume. Felipe, A., Snyders, D.J., Deal, K.K., Tamkun, M.M. Am. J. Physiol. (1993) [Pubmed]
WikiGenes - Universities