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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Calcium-sensing mechanism in TRPC5 channels contributing to retardation of neurite outgrowth.

The calcium- and sodium-permeable transient receptor potential channel TRPC5 has an inhibitory role in neuronal outgrowth but the mechanisms governing its activity are poorly understood. Here we propose a mechanism involving the neuronal calcium sensor-1 (NCS-1) protein. Inhibitory mutants of TRPC5 and NCS-1 enhance neurite outgrowth similarly. Mutant NCS-1 does not inhibit surface-expression of TRPC5 but generally suppresses channel activity, irrespective of whether it is evoked by carbachol, store depletion, lanthanides or elevated intracellular calcium. NCS-1 and TRPC5 are in the same protein complex in rat brain and NCS-1 directly binds to the TRPC5 C-terminus. The data suggest protein-protein interaction between NCS-1 and TRPC5, and involvement of this protein complex in retardation of neurite outgrowth.[1]

References

  1. Calcium-sensing mechanism in TRPC5 channels contributing to retardation of neurite outgrowth. Hui, H., McHugh, D., Hannan, M., Zeng, F., Xu, S.Z., Khan, S.U., Levenson, R., Beech, D.J., Weiss, J.L. J. Physiol. (Lond.) (2006) [Pubmed]
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