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The protein encoded by TRPC6 forms a receptor-activated calcium channel in the cell membrane. Additionally we are shipping Transient Receptor Potential Cation Channel, Subfamily C, Member 6 Antibodies (134) and Transient Receptor Potential Cation Channel, Subfamily C, Member 6 Kits (6) and many more products for this protein.
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Reduction of TRPC6 activity, using either TRPC6 siRNA or a TRPC6 blocker, led to inhibition of hypoxia-induced autophagy, while enhancement of TRPC6 activity with a TRPC6 activator resulted in increased hypoxia-induced autophagy.
axonal colocalization of TRPV4 (show TRPV4 Proteins) and TRPC6 was found in the digital Meissner corpuscles
Data suggest that TRPC6-mediated elevation of intracellular Ca2 (show CA2 Proteins)+ stimulates non-small cell lung cancer proliferation by promoting cell cycle progression.
potential implications of transient receptor potential (TRP) channels in the pathogenesis of intestinal fibrosis, since they are known to act as cellular stress sensors/transducers affecting intracellular Ca(2 (show CA2 Proteins)+) homeostasis/dynamics, and are involved in a broad spectrum of cell pathophysiology including inflammation and tissue remodeling.
Studies provide evidence that the TRPC6-mediated signaling pathway in kidney cells is under control of reactive oxygen species under both physiological and pathological conditions. [review]
SARAF (show TMEM66 Proteins) modulates TRPC1 (show TRPC1 Proteins), but not TRPC6, channel function in a STIM1 (show STIM1 Proteins)-independent manner
Functional interaction of upregulated CaSR (show CASR Proteins) and upregulated TRPC6 in pulmonary artery smooth muscle cells from idiopathic pulmonary arterial hypertension patients may play an important role in the development and progression of sustained pulmonary vasoconstriction and pulmonary vascular remodeling.
Our comprehensive analysis of human disease-causing TRPC6 mutations reveals loss of TRPC6 function as an additional concept of hereditary focal segmental glomerulosclerosis and provides molecular insights into the mechanism responsible for the loss-of-function phenotype of TRPC6 G757D in humans
study demonstrated that the various mechanisms regulating MDR in HCC (show FAM126A Proteins) cells are calcium dependent through the TRPC6/calcium/STAT3 (show STAT3 Proteins) pathway. We propose that targeting TRPC6 in HCC (show FAM126A Proteins) may be a novel antineoplastic strategy, especially combined with chemotherapy
n response to stretching (20%), ATP was released only from the foremost cells at the wound edge; it then diffused to the cells behind the wound edge and activated the P2Y (show P2RY1 Proteins) receptors, which caused propagating Ca(2 (show CA2 Proteins)+) waves via TRPC6
We conclude that TRPC6 channels of pancreatic stellate cells are major effector proteins in an autocrine stimulation pathway triggered by hypoxia.
findings link Trpc6-mediated Ca2 (show CA2 Proteins)+ signaling and nitrosative stress in the redox pathobiology of Duchenne muscular dystrophy (show DMD Proteins)
The injury phase after myocardial infarcts occurs during reperfusion and is a consequence of calcium release from internal stores combined with calcium entry, leading to cell death. We identify canonical transient receptor potential channels (TRPC) 3/6/7 as the cation channels through which most of the damaging calcium enters cells to trigger their death, and we describe mechanisms activated during the injury phase.
Administration of soluble klotho (show KL Proteins) significantly reduced obstruction-induced renal fibrosis in wild-type mice, but not in Trpc6 knockout mice, indicating that klotho (show KL Proteins) and TRPC6 inhibition act in the same pathway to protect against obstruction-induced renal fibrosis.
In the present study, we have explored the hypothesis that TRPC3 (show TRPC3 Proteins) and TRPC6 channels expressed in VSMCs may have a differential contribution to the regulation of vascular tone, which could be relevant for the changes in vascular reactivity associated with essential hypertension
This study demonstrated that Transient Receptor Potential Canonical 6 (TRPC6) and Orai2 (show ORAI2 Proteins) form stromal interaction molecule 2 (STIM2 (show Stim2 Proteins))-regulated neuronal-store-operated Ca(2 (show CA2 Proteins)+) influx (nSOC) channel complex in hippocampal synapse and the resulting Ca(2 (show CA2 Proteins)+) influx is critical for long-term maintenance of mushroom spines in hippocampal neurons.
ASIV may prevent HG-induced podocyte apoptosis via downregulation of TRPC6, which is possibly mediated via the calcineurin/NFAT (show NFATC1 Proteins) signaling pathway.
the mTORC2 (show CRTC2 Proteins)/Akt (show AKT1 Proteins)/NFkappaB pathway-mediated activation of TRPC6 participates in adriamycin-induced podocyte apoptosis.
AngII-injured podocyte had a significant increase in apoptosis, while silencing TRPC6 could decrease the apoptosis induced by AngII.
TRPC3 (show TRPC3 Proteins) and TRPC6 participate diversely in synaptic reorganization in the mossy fiber pathway in temporal lobe epilepsy.
These findings suggest that lysoPC induces CaM (show KRIT1 Proteins) phosphorylation at Tyr (show TYR Proteins)(99) by a Src (show SRC Proteins) family kinase and that phosphorylated CaM (show KRIT1 Proteins) activates PI3K to produce PIP3, which promotes TRPC6 translocation to the cell membrane.
analysis of a TRPC6-TRPC5 (show TRPC5 Proteins) channel cascade that restricts endothelial cell movement
Hyperforin (HF)-induced TRPC6 channel activation increased [Ca(2 (show CA2 Proteins)+)]i concentration, inhibited proliferation, and triggered apoptosis in primary neonatal pig glomerular mesangial cells. This apoptosis was not associated with oxidative stress. Activation stimulated NFATc1 (show NFATC1 Proteins) nuclear translocation. HF also increased FasL (show FASL Proteins) level and caspase-8 (show CASP8 Proteins) activity.
Data found that the pig adrenal medulla expressed predominantly TRPC1 (show TRPC1 Proteins), TRPC5 (show TRPC5 Proteins), and TRPC6 transcripts. The expression level of these TRPCs was significantly elevated in the adrenal medulla from pigs with metabolic syndrome.
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).
, short transient receptor potential channel 6
, transient receptor protein 6
, calcium entry channel
, transient receptor potential cation channel, subfamily C, member 6
, transient receptor potential channel subfamily C member 6
, short transient receptor potential channel 6-like