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Pflugers Arch
2005 Aug 01;4505:345-54. doi: 10.1007/s00424-005-1419-1.
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Inhibition of TRPC5 channels by Ca2+-binding protein 1 in Xenopus oocytes.
Kinoshita-Kawada M
,
Tang J
,
Xiao R
,
Kaneko S
,
Foskett JK
,
Zhu MX
.
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The transient receptor potential canonical type 5 (TRPC5) channel is a member of the channels that has been implicated in neurite extension and growth cone morphology of hippocampal neurons. Although homomeric TRPC5 channels are activated following stimulation of G(q/11)-coupled receptors, the exact mechanism for this activation remains unresolved. Using two-electrode voltage clamp recordings, we show that the activity of TRPC5 channels expressed in Xenopus oocytes is dependent on the presence of Ca2+ at the extracellular as well as the cytoplasmic side of the plasma membrane. TRPC5 was activated by the stimulation of coexpressed M5 muscarinic receptors or by ionomycin. The TRPC5 activity was detectable with the presence of submillimolar levels of extracellular Ca2+, but it was eliminated by the injection of 5 mM 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid into the oocytes. Lanthanum could substitute for extracellular Ca2+ to support TRPC5 activity. Coexpression of Ca2+-binding protein 1 (CaBP1), but not calmodulin (CaM), inhibited the TRPC5 activity, without affecting the cell surface expression of TRPC5 proteins. Using in vitro binding assays, we demonstrated direction interactions between CaBP1 and TRPC5. The CaBP1-binding sites at the C terminus of TRPC5 are closely localized, but not identical, to CaM-binding sites. We conclude that TRPC5 is a Ca2+-regulated channel, and its activity is negatively controlled by CaBP1.
Burgoyne,
The neuronal calcium sensor family of Ca2+-binding proteins.
2001, Pubmed
Burgoyne,
The neuronal calcium sensor family of Ca2+-binding proteins.
2001,
Pubmed
Clapham,
The TRP ion channel family.
2001,
Pubmed
Greka,
TRPC5 is a regulator of hippocampal neurite length and growth cone morphology.
2003,
Pubmed
Haeseleer,
Five members of a novel Ca(2+)-binding protein (CABP) subfamily with similarity to calmodulin.
2000,
Pubmed
Haynes,
Calcium-binding protein 1 is an inhibitor of agonist-evoked, inositol 1,4,5-trisphosphate-mediated calcium signaling.
2004,
Pubmed
Hofmann,
Direct activation of human TRPC6 and TRPC3 channels by diacylglycerol.
1999,
Pubmed
Jung,
Lanthanides potentiate TRPC5 currents by an action at extracellular sites close to the pore mouth.
2003,
Pubmed
Kanki,
Activation of inositol 1,4,5-trisphosphate receptor is essential for the opening of mouse TRP5 channels.
2001,
Pubmed
,
Xenbase
Kasri,
Regulation of InsP3 receptor activity by neuronal Ca2+-binding proteins.
2004,
Pubmed
,
Xenbase
Konstas,
The gamma-subunit of ENaC is more important for channel surface expression than the beta-subunit.
2003,
Pubmed
,
Xenbase
Lambers,
Regulation of the mouse epithelial Ca2(+) channel TRPV6 by the Ca(2+)-sensor calmodulin.
2004,
Pubmed
,
Xenbase
Lee,
Differential modulation of Ca(v)2.1 channels by calmodulin and Ca2+-binding protein 1.
2002,
Pubmed
Liu,
Trp1, a candidate protein for the store-operated Ca(2+) influx mechanism in salivary gland cells.
2000,
Pubmed
Montell,
The TRP channels, a remarkably functional family.
2002,
Pubmed
Niemeyer,
Competitive regulation of CaT-like-mediated Ca2+ entry by protein kinase C and calmodulin.
2001,
Pubmed
Numazaki,
Structural determinant of TRPV1 desensitization interacts with calmodulin.
2003,
Pubmed
Okada,
Molecular cloning and functional characterization of a novel receptor-activated TRP Ca2+ channel from mouse brain.
1998,
Pubmed
Okada,
Molecular and functional characterization of a novel mouse transient receptor potential protein homologue TRP7. Ca(2+)-permeable cation channel that is constitutively activated and enhanced by stimulation of G protein-coupled receptor.
1999,
Pubmed
Parekh,
Store depletion and calcium influx.
1997,
Pubmed
Philipp,
A novel capacitative calcium entry channel expressed in excitable cells.
1998,
Pubmed
Prawitt,
TRPM5 is a transient Ca2+-activated cation channel responding to rapid changes in [Ca2+]i.
2003,
Pubmed
Putney,
Capacitative calcium entry revisited.
1990,
Pubmed
Schaefer,
Receptor-mediated regulation of the nonselective cation channels TRPC4 and TRPC5.
2000,
Pubmed
Strotmann,
Ca2+-dependent potentiation of the nonselective cation channel TRPV4 is mediated by a C-terminal calmodulin binding site.
2003,
Pubmed
Strübing,
TRPC1 and TRPC5 form a novel cation channel in mammalian brain.
2001,
Pubmed
Tang,
Identification of common binding sites for calmodulin and inositol 1,4,5-trisphosphate receptors on the carboxyl termini of trp channels.
2001,
Pubmed
Tang,
Association of mammalian trp4 and phospholipase C isozymes with a PDZ domain-containing protein, NHERF.
2000,
Pubmed
Trebak,
Signaling mechanism for receptor-activated canonical transient receptor potential 3 (TRPC3) channels.
2003,
Pubmed
Vazquez,
Expression level of the canonical transient receptor potential 3 (TRPC3) channel determines its mechanism of activation.
2003,
Pubmed
Yang,
Identification of a family of calcium sensors as protein ligands of inositol trisphosphate receptor Ca(2+) release channels.
2002,
Pubmed
,
Xenbase
Zeng,
Human TRPC5 channel activated by a multiplicity of signals in a single cell.
2004,
Pubmed
Zerangue,
A new ER trafficking signal regulates the subunit stoichiometry of plasma membrane K(ATP) channels.
1999,
Pubmed
,
Xenbase
Zhang,
Activation of Trp3 by inositol 1,4,5-trisphosphate receptors through displacement of inhibitory calmodulin from a common binding domain.
2001,
Pubmed
Zhou,
Ca2+-binding protein-1 facilitates and forms a postsynaptic complex with Cav1.2 (L-type) Ca2+ channels.
2004,
Pubmed
Zhu,
Receptor-activated Ca2+ influx via human Trp3 stably expressed in human embryonic kidney (HEK)293 cells. Evidence for a non-capacitative Ca2+ entry.
1998,
Pubmed
Zhu,
trp, a novel mammalian gene family essential for agonist-activated capacitative Ca2+ entry.
1996,
Pubmed
