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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 Proteins (8) and Transient Receptor Potential Cation Channel, Subfamily C, Member 6 Kits (6) and many more products for this protein.
Showing 10 out of 134 products:
Human Polyclonal TRPC6 Primary Antibody for IP, ELISA - ABIN314245
Foller, Kasinathan, Koka, Lang, Shumilina, Birnbaumer, Lang, Huber: TRPC6 contributes to the Ca(2+) leak of human erythrocytes. in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 2008
Show all 4 Pubmed References
Mouse (Murine) Polyclonal TRPC6 Primary Antibody for FACS, ELISA - ABIN269792
Winn, Conlon, Lynn, Farrington, Creazzo, Hawkins, Daskalakis, Kwan, Ebersviller, Burchette, Pericak-Vance, Howell, Vance, Rosenberg: A mutation in the TRPC6 cation channel causes familial focal segmental glomerulosclerosis. in Science (New York, N.Y.) 2005
axonal colocalization of TRPV4 (show TRPV4 Antibodies) and TRPC6 was found in the digital Meissner corpuscles
Data suggest that TRPC6-mediated elevation of intracellular Ca2 (show CA2 Antibodies)+ 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 (show CA2 Antibodies)+) 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 (show TMEM66 Antibodies) modulates TRPC1 (show TRPC1 Antibodies), but not TRPC6, channel function in a STIM1 (show STIM1 Antibodies)-independent manner
Functional interaction of upregulated CaSR (show CASR Antibodies) 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 (show FAM126A Antibodies) cells are calcium dependent through the TRPC6/calcium/STAT3 (show STAT3 Antibodies) pathway. We propose that targeting TRPC6 in HCC (show FAM126A Antibodies) may be a novel antineoplastic strategy, especially combined with chemotherapy
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 (show P2RY1 Antibodies) receptors, which caused propagating Ca(2 (show CA2 Antibodies)+) waves via TRPC6
Data suggest that targeted manipulation of protein kinase C (show PKC Antibodies) isoforms PKCalpha (show PKCa Antibodies), 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.
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 (show CA2 Antibodies)+ signaling and nitrosative stress in the redox pathobiology of Duchenne muscular dystrophy (show DMD Antibodies)
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 (show KL Antibodies) significantly reduced obstruction-induced renal fibrosis in wild-type mice, but not in Trpc6 knockout mice, indicating that klotho (show KL Antibodies) 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 (show TRPC3 Antibodies) 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 (show ORAI2 Antibodies) form stromal interaction molecule 2 (STIM2 (show Stim2 Antibodies))-regulated neuronal-store-operated Ca(2 (show CA2 Antibodies)+) influx (nSOC) channel complex in hippocampal synapse and the resulting Ca(2 (show CA2 Antibodies)+) 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 (show NFATC1 Antibodies) signaling pathway.
the mTORC2 (show CRTC2 Antibodies)/Akt (show AKT1 Antibodies)/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 (show TRPC3 Antibodies) and TRPC6 participate diversely in synaptic reorganization in the mossy fiber pathway in temporal lobe epilepsy.
These findings suggest that lysoPC induces CaM (show KRIT1 Antibodies) phosphorylation at Tyr (show TYR Antibodies)(99) by a Src (show SRC Antibodies) family kinase and that phosphorylated CaM (show KRIT1 Antibodies) activates PI3K to produce PIP3, which promotes TRPC6 translocation to the cell membrane.
analysis of a TRPC6-TRPC5 (show TRPC5 Antibodies) channel cascade that restricts endothelial cell movement
Hyperforin (HF)-induced TRPC6 channel activation increased [Ca(2 (show CA2 Antibodies)+)]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 (show NFATC1 Antibodies) nuclear translocation. HF also increased FasL (show FASL Antibodies) level and caspase-8 (show CASP8 Antibodies) activity.
Data found that the pig adrenal medulla expressed predominantly TRPC1 (show TRPC1 Antibodies), TRPC5 (show TRPC5 Antibodies), 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