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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Transient receptor potential cation channel, subfamily C, member 6

Trp6, TRPC6
The protein encoded by this gene forms a receptor-activated calcium channel in the cell membrane. The channel is activated by diacylglycerol and is thought to be under the control of a phosphatidylinositol second messenger system. Activation of this channel occurs independently of protein kinase C and is not triggered by low levels of intracellular calcium. Defects in this gene are a cause of focal segmental glomerulosclerosis 2 (FSGS2). [provided by RefSeq, Mar 2009] (from NCBI)
Top mentioned proteins: TRPC3, TRPC1, V1a, TRPC4, CAN
Papers on Trp6
Localized signals that regulate transendothelial migration.
Muller, United States. In Curr Opin Immunol, Feb 2016
Calcium enters through the cation channel TRPC6 and recruits the first wave of trafficking of membrane from the lateral border recycling compartment (LBRC).
Screening of TRPC Channel Activators Identifies Novel Neurotrophic Piperazine Compounds.
Mori et al., Kyoto, Japan. In Mol Pharmacol, Feb 2016
Among the TRPC subfamily, TRPC3 and TRPC6 channels activated directly by diacylglycerol (DAG) play important roles in brain-derived neurotrophic factor (BDNF) signaling, promoting neuronal development and survival.
Danshensu protects against ischemia/reperfusion injury and inhibits the apoptosis of H9c2 cells by reducing the calcium overload through the p-JNK-NF-κB-TRPC6 pathway.
Li et al., Hefei, China. In Int J Mol Med, Jan 2016
The protein expression levels of JNK, phosphorylated (p-)JNK, nuclear factor-κB (NF-κB) and transient receptor potential cation channel, subfamily C, member 6 (TRPC6) were measured by western blot analysis.
Mibefradil suppresses the proliferation of pulmonary artery smooth muscle cells.
Shen et al., Shanghai, China. In J Investig Med, Jan 2016
Transient receptor potential Ca(2+) channel 6 (TRPC6) expression was significantly increased with PDGF-BB stimulation (p=0.009);
TRPC6 is required for hypoxia‑induced basal intracellular calcium concentration elevation, and for the proliferation and migration of rat distal pulmonary venous smooth muscle cells.
Tang et al., Nanjing, China. In Mol Med Report, Jan 2016
The results of the present study demonstrated that TRPC6 was increased in the distal PVs of CHPH rats, and in PVSMCs exposed to hypoxic conditions (4% O2, 72 h); however, TRPC1 was not.
Using Phos-Tag in Western Blotting Analysis to Evaluate Protein Phosphorylation.
Miwa et al., Japan. In Methods Mol Biol, Dec 2015
Here, we describe our method, which is based on in vitro kinase assay and Western blotting analysis using biotinylated Phos-tag and horseradish peroxidase-conjugated streptavidin, to determine the sites of TRPC6 (transient receptor potential canonical 6) channel phosphorylated by protein kinase A.
Calcium, TRPC channels, and regulation of the actin cytoskeleton in podocytes: towards a future of targeted therapies.
Greka et al., Boston, United States. In Pediatr Nephrol, Nov 2015
The identification of the two Ca(2+) permeant channels TRPC5 and TRPC6 as mediators of this pathway not only bolstered the importance of podocyte cytoskeleton dynamics but also revealed promising drug targets for treatment-resistant nephrotic syndrome.
Regulation of TRPC6 ion channels in podocytes - Implications for focal segmental glomerulosclerosis and acquired forms of proteinuric diseases.
Bíró et al., Debrecen, Hungary. In Acta Physiol Hung, Sep 2015
Mutations of the transient receptor potential canonical-6 (TRPC6), a non-selective cation channel that is directly activated by diacylglycerol (DAG), cause a particularly aggressive form of FSGS.
Significant roles of anti-aging protein klotho and fibroblast growth factor23 in cardiovascular disease.
Ma et al., Chongqing, China. In J Geriatr Cardiol, Jul 2015
Recent experiments show that klotho may reduce transient receptor potential canonical6 (TRPC6) channels, resulting in protecting the heart from hypertrophy and systolic dysfunction.
Focal segmental glomerulosclerosis: molecular genetics and targeted therapies.
Liapis et al., Saint Louis, United States. In Bmc Nephrol, 2014
Recent advances show that human focal segmental glomerulosclerosis (FSGS) is a primary podocytopathy caused by podocyte-specific gene mutations including NPHS1, NPHS2, WT-1, LAMB2, CD2AP, TRPC6, ACTN4 and INF2.
Pulsatile atheroprone shear stress affects the expression of transient receptor potential channels in human endothelial cells.
Tepel et al., Berlin, Germany. In Hypertension, 2012
Data show the expression of TRPC6 and TRPV1 was significantly increased after 24 hours of exposure to an atheroprone flow, whereas the expression of TRPC3 and TRPM7 was significantly higher in endothelial cells exposed to shear stress.
Involvement of phosphoinositide 3-kinase and PTEN protein in mechanism of activation of TRPC6 protein in vascular smooth muscle cells.
Boulay et al., Sherbrooke, Canada. In J Biol Chem, 2012
PI3K/PTEN pathway plays an important role in the translocation of TRPC6 to the plasma membrane and may thus have a significant impact on Ca(2+) signaling in cells that endogenously express TRPC6.
The upregulation of TRPC6 contributes to Ca²⁺ signaling and actin assembly in human mesangial cells after chronic hypoxia.
Jiao et al., Harbin, China. In Biochem Biophys Res Commun, 2012
the upregulation of TRPC6 is involved in the Ca(2+) signaling and actin assembly in human mesangial cells after chronic hypoxia.
Activation of TRPC6 channels is essential for lung ischaemia-reperfusion induced oedema in mice.
Dietrich et al., Gießen, Germany. In Nat Commun, 2011
TRPC6 channel activation is essential for lung ischaemia-reperfusion induced oedema in mice
Expression of TRPC6 in renal cortex and hippocampus of mouse during postnatal development.
Yang et al., Tianjin, China. In Plos One, 2011
Developmental changes in TRPC6 expression might be required for proper postnatal development of the hippocampus and the kidney cortex.
Melanopsin signalling in mammalian iris and retina.
Yau et al., Baltimore, United States. In Nature, 2011
Ablating in mouse the expression of both TRPC6 and TRPC7, members of the TRP channel superfamily, also essentially eliminated the M1-ipRGC light response but the intrinsic PLR was not affected.
STIM1 heteromultimerizes TRPC channels to determine their function as store-operated channels.
Muallem et al., Dallas, United States. In Nat Cell Biol, 2007
Through a distinct mechanism, STIM1 also regulates TRPC3 and TRPC6.
TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function.
Pollak et al., Boston, United States. In Nat Genet, 2005
the canonical transient receptor potential 6 (TRPC6) ion channel is expressed in podocytes and is a component of the glomerular slit diaphragm.
A mutation in the TRPC6 cation channel causes familial focal segmental glomerulosclerosis.
Rosenberg et al., Durham, United States. In Science, 2005
a family with familial focal segmental glomerulosclerosis carries a missense mutation in TRPC6; the proline-to-glutamine substitution enhances TRPC6-mediated calcium signals in response to agonists & appears to alter intracellular distribution of TRPC6
Essential role of TRPC channels in the guidance of nerve growth cones by brain-derived neurotrophic factor.
Yuan et al., Shanghai, China. In Nature, 2005
Several members of the TRPC family are highly expressed in these neurons, and both Ca2+ elevation and growth-cone turning induced by BDNF are abolished by pharmacological inhibition of TRPC channels, overexpression of a dominant-negative form of TRPC3 or TRPC6, or downregulation of TRPC3 expression via short interfering RNA.
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