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Calcium‐sensing mechanism in TRPC5 channels contributing to retardation of neurite outgrowth
Author(s) -
Hui Hui,
McHugh Damian,
Hannan Meredith,
Zeng Fanning,
Xu ShangZhong,
Khan SaeedulHassan,
Levenson Robert,
Beech David J.,
Weiss Jamie L.
Publication year - 2006
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2005.102889
Subject(s) - trpc5 , neurite , chemistry , microbiology and biotechnology , transient receptor potential channel , calcium in biology , biophysics , mutant , inhibitory postsynaptic potential , carbachol , calcium , biochemistry , intracellular , trpc , receptor , neuroscience , biology , in vitro , gene , organic chemistry
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.