Date of this Version
Published in Cerebellum 1:2 (2002), pp. 103–109; doi: 10.1080/147342202753671231.
Taurine efflux occurs in association with cell swelling in both hyposmotic and isosmotic conditions and during cell shrinkage in apoptotic death. Release occurs through a leak pathway, is largely Ca2+-independent and is sensitive to Cl– channel blockers. Taurine efflux elicited by hyposmolarity is reduced or suppressed by tyrosine kinase blockers and increased by tyrosine phosphatase inhibitors. The specific kinases involved are still unknown and may be different in the various cell types. Non-receptor and scr-related protein kinases have been identified in some cells as elements that directly phosphorylate the taurine efflux pathway. Possible tyrosine kinase targets are the phosphinositide kinase (PI3K), which if inhibited, prevents the osmosensitive taurine efflux in brain cells, or the small GTP-binding proteins associated with remodeling of the cytoskeleton. The similar effects of tyrosine kinase modulators on volume-activated taurine fluxes and Cl– currents are suggestive of either a shared translocation pathway or a common step in the signaling network. The effects of tyrosine kinases on taurine efflux activated in isosmotic swelling and in the release associated with apoptosis are essentially unexplored.
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