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The protein encoded by TRPC6 forms a receptor-activated calcium channel in the cell membrane. 再加上，我们可以发Transient Receptor Potential Cation Channel, Subfamily C, Member 6 蛋白 (8) 和 Transient Receptor Potential Cation Channel, Subfamily C, Member 6 试剂盒 (6)和数多这个蛋白质的别的产品。
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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
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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
These findings suggest that lysoPC induces CaM (显示 KRIT1 抗体) phosphorylation at Tyr (显示 TYR 抗体)(99) by a Src (显示 SRC 抗体) family kinase and that phosphorylated CaM (显示 KRIT1 抗体) activates PI3K to produce PIP3, which promotes TRPC6 translocation to the cell membrane.
analysis of a TRPC6-TRPC5 (显示 TRPC5 抗体) channel cascade that restricts endothelial cell movement
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 (显示 CA2 抗体)+) 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 (显示 TMEM66 抗体) modulates TRPC1 (显示 TRPC1 抗体), but not TRPC6, channel function in a STIM1 (显示 STIM1 抗体)-independent manner
Functional interaction of upregulated CaSR (显示 CASR 抗体) 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 (显示 FAM126A 抗体) cells are calcium dependent through the TRPC6/calcium/STAT3 (显示 STAT3 抗体) pathway. We propose that targeting TRPC6 in HCC (显示 FAM126A 抗体) 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 (显示 P2RY1 抗体) receptors, which caused propagating Ca(2 (显示 CA2 抗体)+) waves via TRPC6
Data suggest that targeted manipulation of protein kinase C (显示 PKC 抗体) isoforms PKCalpha (显示 PKCa 抗体), 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.
Insulin increases the expression of TRPC6 channels in podocytes by activation of the calcineurin-dependent pathway.
This study described the expression and functional relevance of TRPC6 in the pathophysiology of HK-2 (显示 HK2 抗体) cell following ischemia reperfusion.
Administration of soluble klotho (显示 KL 抗体) significantly reduced obstruction-induced renal fibrosis in wild-type mice, but not in Trpc6 knockout mice, indicating that klotho (显示 KL 抗体) 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 (显示 TRPC3 抗体) 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 (显示 ORAI2 抗体) form stromal interaction molecule 2 (STIM2 (显示 Stim2 抗体))-regulated neuronal-store-operated Ca(2 (显示 CA2 抗体)+) influx (nSOC) channel complex in hippocampal synapse and the resulting Ca(2 (显示 CA2 抗体)+) 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 (显示 NFATC1 抗体) signaling pathway.
the mTORC2 (显示 CRTC2 抗体)/Akt (显示 AKT1 抗体)/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 (显示 TRPC3 抗体) 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.
Selectively activating endothelial TRPC6 rescues transendothelial migration
MicroRNA-26a prevents endothelial cell apoptosis by directly targeting TRPC6 in the setting of atherosclerosis.
Data found that the pig adrenal medulla expressed predominantly TRPC1 (显示 TRPC1 抗体), TRPC5 (显示 TRPC5 抗体), 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