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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 (121) and Transient Receptor Potential Cation Channel, Subfamily C, Member 6 Proteins (7) and many more products for this protein.
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These findings suggest that lysoPC induces CaM (show KRIT1 ELISA Kits) phosphorylation at Tyr (show TYR ELISA Kits)(99) by a Src (show SRC ELISA Kits) family kinase and that phosphorylated CaM (show KRIT1 ELISA Kits) activates PI3K to produce PIP3, which promotes TRPC6 translocation to the cell membrane.
analysis of a TRPC6-TRPC5 (show TRPC5 ELISA Kits) channel cascade that restricts endothelial cell movement
Genetic Interactions Between TRPC6 and NPHS1 (show NPHS1 ELISA Kits) Variants Affect Posttransplant Risk of Recurrent Focal Segmental Glomerulosclerosis.
These findings suggest that lysoPC induces CaM (show CALM1 ELISA Kits) phosphorylation at Tyr (show TYR ELISA Kits)(99) by a Src (show SRC ELISA Kits) family kinase and that phosphorylated CaM (show CALM1 ELISA Kits) activates PI3K (show PIK3CA ELISA Kits) to produce PIP3, which promotes TRPC6 translocation to the cell membrane.
This study demonstrated that TRPC6 reduction or haploinsufficiency leads to altered neuronal development, morphology and function.
TRPC6 specifically interacts with APP (show APP ELISA Kits) leading to inhibition of its cleavage by gamma-secretase and reduction in Abeta (show APP ELISA Kits) production.
results suggest that TRPC6 regulates metabolism to affect HIF-1alpha (show HIF1A ELISA Kits) stability and consequent glucose metabolism in human glioma cells under hypoxia
HIF-1alpha (show HIF1A ELISA Kits) knockdown attenuated hypoxia-induced BMP4 (show BMP4 ELISA Kits) expression and knockdown of either HIF-1alpha (show HIF1A ELISA Kits) or BMP4 (show BMP4 ELISA Kits) abolished hypoxia-induced TRPC expression and basal [Ca(2 (show CA2 ELISA Kits)+)]i.
TRPC3 (show TRPC3 ELISA Kits) and TRPC6 participate diversely in synaptic reorganization in the mossy fiber pathway in temporal lobe epilepsy.
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.
TRPC6 genetic variants are promising candidate predictors of nervous system involvement in systemic lupus erythematosus
Selectively activating endothelial TRPC6 rescues transendothelial migration
AngII-injured podocyte had a significant increase in apoptosis, while silencing TRPC6 could decrease the apoptosis induced by AngII.
MicroRNA-26a prevents endothelial cell apoptosis by directly targeting TRPC6 in the setting of atherosclerosis.
These findings indicate that the mTORC2 (show CRTC2 ELISA Kits) signaling pathway regulates TRPC6 in podocytes but that the mTORC1 signaling pathway does not appear to exert an effect on TRPC6.
these findings provide strong evidence for a role of immunophilins, including FKBP25 (show FKBP3 ELISA Kits) and FKBP38 (show FKBP8 ELISA Kits), in NCCE mediated by TRPC6.
Locally generated Sdc4 (show SDC4 ELISA Kits) may play a role in regulating TRPC6 channels, and may contribute to glomerular pathology.
Results suggest that stretch-accelerated wound closure is due to the ATP release through mechanosensitive hemichannels from the foremost cells and the subsequent Ca(2 (show CA2 ELISA Kits)+) waves mediated by P2Y (show P2RY1 ELISA Kits) and TRPC6 activation.
Results suggest that IL-17A (show IL17A ELISA Kits) may promote brain ischemia reperfusion injury through the increase of calpain-mediated TRPC6 proteolysis
Data found that the pig adrenal medulla expressed predominantly TRPC1 (show TRPC1 ELISA Kits), TRPC5 (show TRPC5 ELISA Kits), 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).
transient receptor potential cation channel, subfamily C, member 6
, short transient receptor potential channel 6-like
, short transient receptor potential channel 6
, transient receptor protein 6
, calcium entry channel
, transient receptor potential channel subfamily C member 6