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The protein encoded by TRPC6 forms a receptor-activated calcium channel in the cell membrane. 再加上，我们可以发Transient Receptor Potential Cation Channel, Subfamily C, Member 6 抗体 (134) 和 Transient Receptor Potential Cation Channel, Subfamily C, Member 6 试剂盒 (6)和数多这个蛋白质的别的产品。
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Confirmed serine 14 as a target of MAPKs and proline-directed kinases like cyclin-dependent kinase 5 (Cdk5 (显示 CDK5 蛋白)) in cell-based as well as in vitro kinase assays and quantitative phosphoproteomic analysis of TRPC6. Phosphorylation of TRPC6 at serine 14 enhances channel conductance by boosting membrane expression of TRPC6, whereas protein stability and multimerization of TRPC6 are not altered.
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 (显示 TRPV4 蛋白) and TRPC6 was found in the digital Meissner corpuscles
Data suggest that TRPC6-mediated elevation of intracellular Ca2 (显示 CA2 蛋白)+ 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 (显示 CA2 蛋白)+) 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 (显示 TMEM66 蛋白) modulates TRPC1 (显示 TRPC1 蛋白), but not TRPC6, channel function in a STIM1 (显示 STIM1 蛋白)-independent manner
Functional interaction of upregulated CaSR (显示 CASR 蛋白) 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 (显示 FAM126A 蛋白) cells are calcium dependent through the TRPC6/calcium/STAT3 (显示 STAT3 蛋白) pathway. We propose that targeting TRPC6 in HCC (显示 FAM126A 蛋白) may be a novel antineoplastic strategy, especially combined with chemotherapy
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 (显示 CA2 蛋白)+ signaling and nitrosative stress in the redox pathobiology of Duchenne muscular dystrophy (显示 DMD 蛋白)
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 (显示 KL 蛋白) significantly reduced obstruction-induced renal fibrosis in wild-type mice, but not in Trpc6 knockout mice, indicating that klotho (显示 KL 蛋白) 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 (显示 TRPC3 蛋白) 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 (显示 ORAI2 蛋白) form stromal interaction molecule 2 (STIM2 (显示 Stim2 蛋白))-regulated neuronal-store-operated Ca(2 (显示 CA2 蛋白)+) influx (nSOC) channel complex in hippocampal synapse and the resulting Ca(2 (显示 CA2 蛋白)+) 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 (显示 NFATC1 蛋白) signaling pathway.
the mTORC2 (显示 CRTC2 蛋白)/Akt (显示 AKT1 蛋白)/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 (显示 TRPC3 蛋白) and TRPC6 participate diversely in synaptic reorganization in the mossy fiber pathway in temporal lobe epilepsy.
These findings suggest that lysoPC induces CaM (显示 KRIT1 蛋白) phosphorylation at Tyr (显示 TYR 蛋白)(99) by a Src (显示 SRC 蛋白) family kinase and that phosphorylated CaM (显示 KRIT1 蛋白) activates PI3K to produce PIP3, which promotes TRPC6 translocation to the cell membrane.
analysis of a TRPC6-TRPC5 (显示 TRPC5 蛋白) channel cascade that restricts endothelial cell movement
Hyperforin (HF)-induced TRPC6 channel activation increased [Ca(2 (显示 CA2 蛋白)+)]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 (显示 NFATC1 蛋白) nuclear translocation. HF also increased FasL (显示 FASL 蛋白) level and caspase-8 (显示 CASP8 蛋白) activity.
Data found that the pig adrenal medulla expressed predominantly TRPC1 (显示 TRPC1 蛋白), TRPC5 (显示 TRPC5 蛋白), 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