Functional characterization of beta isoforms of murine Na,K-ATPase. The adhesion molecule on glia (AMOG/beta 2), but not beta 1, promotes neurite outgrowth.
We have previously provided evidence for a dual function of the adhesion molecule on glia (AMOG/beta 2), the beta 2 subunit of the murine Na,K-ATPase, both as neural recognition molecule mediating neuron-glia interactions and as functional beta subunit of the sodium pump. To analyze the functional role of AMOG/beta 2 in neurite outgrowth, AMOG/beta 2-expressing L-cells were generated by transfection and used as substrates for neurite outgrowth of cerebellar and hippocampal neurons. AMOG/beta 2-transfected L-cells led to an increase in neurite length after 6 h, which was specifically inhibited by antibodies to AMOG/beta 2 and a neuronal membrane fraction. Moreover, the extracellular domain of AMOG/beta 2 generated as a soluble recombinant protein in Chinese hamster ovary cells partially inhibited the increase in neurite outgrowth on AMOG/beta 2-transfected L-cells. L-cells transfected with the mouse beta 1 subunit had no effect on neurite extension. Our observations show for the first time differences in functional properties for different beta isoforms of the Na,K-ATPase and suggest that AMOG/beta 2 but not beta 1 is able to interact with an unknown neuronal receptor leading to increased neurite outgrowth, most likely via signal transduction.[1]References
- Functional characterization of beta isoforms of murine Na,K-ATPase. The adhesion molecule on glia (AMOG/beta 2), but not beta 1, promotes neurite outgrowth. Müller-Husmann, G., Gloor, S., Schachner, M. J. Biol. Chem. (1993) [Pubmed]
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