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J Physiol. 2006 Apr 1;572(Pt 1):165-72. Epub 2006 Feb 9.

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

Author information

1
Institute of Membrane and Systems Biology, Garstang Building, University of Leeds, Leeds LS2 9JT, UK.

Abstract

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.

PMID:
16469785
PMCID:
PMC1779652
DOI:
10.1113/jphysiol.2005.102889
[Indexed for MEDLINE]
Free PMC Article

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