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The protein encoded by TRPC3 is a membrane protein that can form a non-selective channel permeable to calcium and other cations. Additionally we are shipping TRPC3 Antibodies (85) and TRPC3 Kits (1) and many more products for this protein.
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Data show clear inhibition of the photouncaging- induced Ca2+ signal by the TRPC3 channel inhibitor SKF 96365.
The subsequent ER stress-induced apoptosis exhibit a strong requirement for constitutive Ca(2+) influx and that TRPC3 contributes to this process.
Data show that mechanical stretching of transient receptor potential cation channel, subfamily C, member 3 (TRPC3) overexpressing fibroblasts induced the activation of nuclear factor-kappa B (NFkappaB).
TRPC3 and TRPC6 (show TRPC6 Proteins) participate diversely in synaptic reorganization in the mossy fiber pathway in temporal lobe epilepsy.
the first in vivo evidence for a proatherogenic role of endothelial TRPC3.
Imin channels are regulated by STIM2 (show Stim2 Proteins), TRPC3-containing INS (show INS Proteins) channels are induced by STIM1 (show STIM1 Proteins), and TRPC1 (show TRPC1 Proteins)-composed Imax channels are activated by both STIM1 (show STIM1 Proteins) and STIM2 (show Stim2 Proteins).
CaSR (show CASR Proteins) activation mediates Ca2 (show CA2 Proteins)+ influx and cell proliferation via TRPC3 and TRPC6 (show TRPC6 Proteins) in human mesangial cells
although gene deletion of TRPC3 or TRPC6 (show TRPC6 Proteins) alone did not protect against hypertrophy or dysfunction from pressure overload, combined deletion was protective, supporting the value of dual inhibition
there is an absolute requirement for TRPC3-mediated diacylglycerol-dependent Ca(2 (show CA2 Proteins)+) entry to initiate and sustain the spiking response.
Removal of a large hydrophobic residue (I667A or I667E) generated TRPC3 channels with approximately 60% constitutive activity, suggesting I667 as part of the dynamic structure occluding the permeation path.
Downregulation of TRPC3 in liver sinusoid endothelial cells reduces their susceptibility to endoplasmic reticulum stress-induced apoptosis.
In the present study, we have explored the hypothesis that TRPC3 and TRPC6 (show TRPC6 Proteins) 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
data suggested Acetylcholine could induce Airway Smooth Muscle Cell proliferation, and TRPC3 may be involved in ACh (show FGFR3 Proteins)-induced ASMC proliferation that occurs with airway remodeling.
The results of this study demonstrated that TRPC3 channels unequivocally contribute to pilocarpine-induced SE and could be a novel molecular target for new anticonvulsive drugs.
Inhibiting TRPC3 with continuous subcutaneous administration of Pyr3 decreased enhanced pause (Penh) of OVA-sensitized mouse. Meanwhile, both Pyr3 and lentiviral shRNA treatment of ASMCs in OVA-sensitized mouse significantly decreased their proliferation and migration
TRPC3 channels are required for the response to glucose of mediobasal hypothalamic glucose-excited neurons and the central effect of glucose on insulin (show INS Proteins) secretion and food intake.
These findings suggest that Trpc3 is a mediator of pathologic cardiac hypertrophy not only through mediating part of the Ca(2 (show CA2 Proteins)+) influx, but also through control of CaV1.2 (show CACNA1C Proteins) expressions.
May activate TRPC3 channels to cause extracellular Ca(2 (show CA2 Proteins)+) influx.
Data suggest that activation of adenosine A1 receptors elicit receptor-operated Ca(2+) entry in porcine afferent arterioles, the level of which is dependent on postnatal maturation of TRPC3 channels.
Demonstrate that Ca(2+) entry via endothelial TRPC3 contributes to nitric oxide release and have revealed that hypoxia-reoxygenation is associated with inhibition of TRPC3 activity.
Study determined the sequence of pig TRPC1 and TRPC3-7 channels and found pig TRPC cDNAs resemble their human homologs more than the others .
heteromeric cation channels comprised of the TRPP2 mutant and the TRPC3 or TRPC7 (show TRPM2 Proteins) protein induce enhanced receptor-activated Ca(2 (show CA2 Proteins)+) influx that may lead to dysregulated cell growth in ADPKD
The protein encoded by this gene is a membrane protein that can form a non-selective channel permeable to calcium and other cations. The encoded protein appears to be induced to form channels by a receptor tyrosine kinase-activated phosphatidylinositol second messenger system and also by depletion of intracellular calcium stores. Two transcript variants encoding different isoforms have been found for this gene.
transient receptor potential cation channel, subfamily C, member 3
, short transient receptor potential channel 3-like
, short transient receptor potential channel 3
, transient receptor protein 3
, receptor-activated cation channel TRP3
, trp-related protein 3
, ion channel protein
, transient receptor potential cation channel subfamily C member 3
, oocyte transient receptor potential channel