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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]
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SARAF modulates TRPC1, but not TRPC6, channel function in a STIM1-independent manner
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Functional interaction of upregulated CaSR 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.
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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
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study demonstrated that the various mechanisms regulating MDR in HCC cells are calcium dependent through the TRPC6/calcium/STAT3 pathway. We propose that targeting TRPC6 in HCC may be a novel antineoplastic strategy, especially combined with chemotherapy
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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 receptors, which caused propagating Ca(2+) waves via TRPC6
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Data suggest that targeted manipulation of protein kinase C isoforms PKCalpha, PKCbeta, and PKCeta might be beneficial in certain proteinuric kidney diseases with altered transient receptor potential cation channel subfamily C member 6 protein (TRPC6) functions.
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Insulin increases the expression of TRPC6 channels in podocytes by activation of the calcineurin-dependent pathway.
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This study described the expression and functional relevance of TRPC6 in the pathophysiology of HK-2 cell following ischemia reperfusion.
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Genetic Interactions Between TRPC6 and NPHS1 Variants Affect Posttransplant Risk of Recurrent Focal Segmental Glomerulosclerosis.
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These findings suggest that lysoPC induces CaM phosphorylation at Tyr(99) by a Src family kinase and that phosphorylated CaM activates PI3K to produce PIP3, which promotes TRPC6 translocation to the cell membrane.
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This study demonstrated that TRPC6 reduction or haploinsufficiency leads to altered neuronal development, morphology and function.
