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TRPC6-mediated Ca(2+) influx plays a novel role in suppressing cytoprotective autophagy triggered by oxidative stress in PTC.
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Studied physiology of transient receptor potential cation channel subfamily C member 6 (TRPC6) in cultured human intervertebral disc cells exposed to simulated microgravity and to the TRPC channel inhibitor SKF-96365. Results found the simulated microgravity and/or TRPC channel inhibition led to reduced proliferation, increased senescence, and reduced TRPC6 expression.
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this study presents the structure of human TRPC6 homotetramer in complex with a newly identified high-affinity inhibitor BTDM solved by single-particle cryo-electron microscopy to 3.8 A resolution.
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In systemic lupus erythematous patients, TRPC6 influenced calcium currents, apoptosis rates and cytokine secretion in a disease- and genotype-dependent manner.
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TRPC6 expression is inversely correlated with cognitive performance of Alzheimer Disease (AD). TRPC6 in peripheral leucocytes may be a potential biomarker for the diagnosis of AD.
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Findings indicate that OLCT impairs the ability of breast cancer cells to proliferate and migrate via downregulation of TRPC6 channel expression while having no effect on the biology of non-tumoral breast cells.
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TRPC6 plays a pro-inflammatory role in the pathogenesis of CRSwNP via regulating Ca(2+) flow. Targeted therapy using TRPC6 inhibitor including SKF-96365 and TRPC6 small interfering RNA (siRNA) intranasally may alleviate the inflammatory reaction in CRSwNP.
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data demonstrate that the direct activation of TRPC6 channels contributes to CNCP-induced apoptotic cell death in HK-2cells
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Four novel TRPC6 variants were detected in Iranian focal segmental glomerulosclerosis children; in silico analysis showed that 2 variants (D130V and G162R) could be pathogenic.
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Authors found a specific reduction of TRPC6 mRNA levels in four AD sets and one MCI set. The median TRPC6 mRNA levels were lower in the following: (1) combined AD patients than in age-matched controls (0.78 vs 1.73, P<0.001); (2) mild-to-moderate AD patients than in age-matched controls (0.81 vs 1.73, P<0.001); and (3) MCI patients than in age-matched controls (0.76 vs 1.72, P<0.001).
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The results strongly suggest that Nox2 destabilization through disrupting TRPC3-Nox2 complex underlies attenuation of hyperglycemia-induced heart failure by TRPC6.
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The underlying mechanism forAT1-autoantibody induced podocyte damage might involve activation of the TRPC6 -calcium/calcineurin pathway.
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TRPC6 was upregulated in Diabetic nephropathy and could promote cell proliferation and inflammation by inhibiting the NFAT signaling pathway in tubular epithelial cells.
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Changes in podocyte TRPC channels evoked by plasma and sera from patients with recurrent FSGS and by putative glomerular permeability factors.
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Confirmed serine 14 as a target of MAPKs and proline-directed kinases like cyclin-dependent kinase 5 (Cdk5) 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.
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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.
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axonal colocalization of TRPV4 and TRPC6 was found in the digital Meissner corpuscles
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Data suggest that TRPC6-mediated elevation of intracellular Ca2+ stimulates non-small cell lung cancer proliferation by promoting cell cycle progression.
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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+) homeostasis/dynamics, and are involved in a broad spectrum of cell pathophysiology including inflammation and tissue remodeling.
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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]