anti-Transient Receptor Potential Cation Channel, Subfamily C, Member 6 (TRPC6) Antibodies

Human Transient Receptor Potential Cation Channel, Subfamily C, Member 6 (TRPC6) interaction partners

1. data demonstrate that the direct activation of TRPC6 channels contributes to CNCP-induced apoptotic cell death in HK-2cells

2. 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.

3. 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).

4. The results strongly suggest that Nox2 destabilization through disrupting TRPC3-Nox2 complex underlies attenuation of hyperglycemia-induced heart failure by TRPC6.

5. The underlying mechanism forAT1-autoantibody induced podocyte damage might involve activation of the TRPC6 -calcium/calcineurin pathway.

6. TRPC6 was upregulated in Diabetic nephropathy and could promote cell proliferation and inflammation by inhibiting the NFAT signaling pathway in tubular epithelial cells.

7. Changes in podocyte TRPC channels evoked by plasma and sera from patients with recurrent FSGS and by putative glomerular permeability factors.

8. 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.

9. 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.

10. axonal colocalization of TRPV4 and TRPC6 was found in the digital Meissner corpuscles

11. Data suggest that TRPC6-mediated elevation of intracellular Ca2+ stimulates non-small cell lung cancer proliferation by promoting cell cycle progression.

12. 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.

13. 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]

14. SARAF modulates TRPC1, but not TRPC6, channel function in a STIM1-independent manner

15. 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.

16. 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

17. 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

18. 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

19. 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.

20. Insulin increases the expression of TRPC6 channels in podocytes by activation of the calcineurin-dependent pathway.

Mouse (Murine) Transient Receptor Potential Cation Channel, Subfamily C, Member 6 (TRPC6) interaction partners

1. results together suggested that miR-200b-3p inhibition reduced the currents of TRPC6, which led to the decrease of intracellular Ca(2+) concentration

2. Trpc3 mRNA expression was significantly elevated in kidneys of Trpc6(-/-) mice underwent unilateral ureteral obstruction (UUO) while the levels did not change in kidneys of neither WT nor in New Zealand obese mice underwent UUO.

3. This work indicates that TRPC6 exerts critical pathophysiological functions in placenta, and provides further evidence for a role of this channel in the homeostasis of cations like Zn and Fe.

4. structure of the cytoplasmic domain of murine transient receptor potential cation channel subfamily C member 6

5. These results suggest that TRPC6 may regulate GFR by modulating MC contractile function through multiple Ca(2+) signaling pathways.

6. TRPC6-/- mice show less collagen production and normal lung function in pulmonary fibrosis compared to wild-type controls. TRPC6 expression is up-regulated in TGF-beta1-induced lung fibroblast-myofibroblast transdifferentiation.

7. We conclude that TRPC6 channels of pancreatic stellate cells are major effector proteins in an autocrine stimulation pathway triggered by hypoxia.

8. findings link Trpc6-mediated Ca2+ signaling and nitrosative stress in the redox pathobiology of Duchenne muscular dystrophy

9. 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.

10. Administration of soluble klotho significantly reduced obstruction-induced renal fibrosis in wild-type mice, but not in Trpc6 knockout mice, indicating that klotho and TRPC6 inhibition act in the same pathway to protect against obstruction-induced renal fibrosis.

11. In the present study, we have explored the hypothesis that TRPC3 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

12. This study demonstrated that Transient Receptor Potential Canonical 6 (TRPC6) and Orai2 form stromal interaction molecule 2 (STIM2)-regulated neuronal-store-operated Ca(2+) influx (nSOC) channel complex in hippocampal synapse and the resulting Ca(2+) influx is critical for long-term maintenance of mushroom spines in hippocampal neurons.

13. ASIV may prevent HG-induced podocyte apoptosis via downregulation of TRPC6, which is possibly mediated via the calcineurin/NFAT signaling pathway.

14. the mTORC2/Akt/NFkappaB pathway-mediated activation of TRPC6 participates in adriamycin-induced podocyte apoptosis.

15. AngII-injured podocyte had a significant increase in apoptosis, while silencing TRPC6 could decrease the apoptosis induced by AngII.

16. transient receptor potential canonical 6 is an essential component of the slit diaphragm and is required for development of glomerulus

17. TRPC3 and TRPC6 participate diversely in synaptic reorganization in the mossy fiber pathway in temporal lobe epilepsy.

18. the transient receptor potential canonical-6 (TRPC6) calcium-permeable channel in the alveolar macrophages also functions to shunt the transmembrane potential generated by proton pumping.

19. Selectively activating endothelial TRPC6 rescues transendothelial migration

20. MicroRNA-26a prevents endothelial cell apoptosis by directly targeting TRPC6 in the setting of atherosclerosis.

Cow (Bovine) Transient Receptor Potential Cation Channel, Subfamily C, Member 6 (TRPC6) interaction partners

1. 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.

2. analysis of a TRPC6-TRPC5 channel cascade that restricts endothelial cell movement

Pig (Porcine) Transient Receptor Potential Cation Channel, Subfamily C, Member 6 (TRPC6) interaction partners

1. Hyperforin (HF)-induced TRPC6 channel activation increased [Ca(2+)]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 nuclear translocation. HF also increased FasL level and caspase-8 activity.

2. Data found that the pig adrenal medulla expressed predominantly TRPC1, TRPC5, and TRPC6 transcripts. The expression level of these TRPCs was significantly elevated in the adrenal medulla from pigs with metabolic syndrome.