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The protein encoded by TRPC6 forms a receptor-activated calcium channel in the cell membrane. Zusätzlich bieten wir Ihnen Transient Receptor Potential Cation Channel, Subfamily C, Member 6 Proteine (8) und Transient Receptor Potential Cation Channel, Subfamily C, Member 6 Kits (6) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal TRPC6 Primary Antibody für 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 für 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 (zeige TRPV4 Antikörper) and TRPC6 was found in the digital Meissner corpuscles
Data suggest that TRPC6-mediated elevation of intracellular Ca2 (zeige CA2 Antikörper)+ 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 (zeige CA2 Antikörper)+) 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 (zeige TMEM66 Antikörper) modulates TRPC1 (zeige TRPC1 Antikörper), but not TRPC6, channel function in a STIM1 (zeige STIM1 Antikörper)-independent manner
Functional interaction of upregulated CaSR (zeige CASR Antikörper) 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 (zeige FAM126A Antikörper) cells are calcium dependent through the TRPC6/calcium/STAT3 (zeige STAT3 Antikörper) pathway. We propose that targeting TRPC6 in HCC (zeige FAM126A Antikörper) 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 (zeige P2RY1 Antikörper) receptors, which caused propagating Ca(2 (zeige CA2 Antikörper)+) waves via TRPC6
Data suggest that targeted manipulation of protein kinase C (zeige PKC Antikörper) isoforms PKCalpha (zeige PKCa Antikörper), 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 (zeige CA2 Antikörper)+ signaling and nitrosative stress in the redox pathobiology of Duchenne muscular dystrophy (zeige DMD Antikörper)
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 (zeige KL Antikörper) significantly reduced obstruction-induced renal fibrosis in wild-type mice, but not in Trpc6 knockout mice, indicating that klotho (zeige KL Antikörper) 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 (zeige TRPC3 Antikörper) 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 (zeige ORAI2 Antikörper) form stromal interaction molecule 2 (STIM2 (zeige Stim2 Antikörper))-regulated neuronal-store-operated Ca(2 (zeige CA2 Antikörper)+) influx (nSOC) channel complex in hippocampal synapse and the resulting Ca(2 (zeige CA2 Antikörper)+) 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 (zeige NFATC1 Antikörper) signaling pathway.
the mTORC2 (zeige CRTC2 Antikörper)/Akt (zeige AKT1 Antikörper)/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 (zeige TRPC3 Antikörper) and TRPC6 participate diversely in synaptic reorganization in the mossy fiber pathway in temporal lobe epilepsy.
These findings suggest that lysoPC induces CaM (zeige KRIT1 Antikörper) phosphorylation at Tyr (zeige TYR Antikörper)(99) by a Src (zeige SRC Antikörper) family kinase and that phosphorylated CaM (zeige KRIT1 Antikörper) activates PI3K to produce PIP3, which promotes TRPC6 translocation to the cell membrane.
analysis of a TRPC6-TRPC5 (zeige TRPC5 Antikörper) channel cascade that restricts endothelial cell movement
Hyperforin (HF)-induced TRPC6 channel activation increased [Ca(2 (zeige CA2 Antikörper)+)]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 (zeige NFATC1 Antikörper) nuclear translocation. HF also increased FasL (zeige FASL Antikörper) level and caspase-8 (zeige CASP8 Antikörper) activity.
Data found that the pig adrenal medulla expressed predominantly TRPC1 (zeige TRPC1 Antikörper), TRPC5 (zeige TRPC5 Antikörper), 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