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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 Proteins (9) and TRPC3 Kits (1) and many more products for this protein.
Showing 10 out of 84 products:
Human Polyclonal TRPC3 Primary Antibody for IHC, ELISA - ABIN1003365
Montell, Birnbaumer, Flockerzi, Bindels, Bruford, Caterina, Clapham, Harteneck, Heller, Julius, Kojima, Mori, Penner, Prawitt, Scharenberg, Schultz, Shimizu, Zhu: A unified nomenclature for the superfamily of TRP cation channels. in Molecular cell 2002
Show all 4 Pubmed References
Human Polyclonal TRPC3 Primary Antibody for IHC, ELISA - ABIN1003364
Dietrich, Kalwa, Rost, Gudermann: The diacylgylcerol-sensitive TRPC3/6/7 subfamily of cation channels: functional characterization and physiological relevance. in Pflügers Archiv : European journal of physiology 2005
Show all 3 Pubmed References
Human Polyclonal TRPC3 Primary Antibody for ELISA, WB - ABIN563263
Aydar, Yeo, Djamgoz, Palmer et al.: Abnormal expression, localization and interaction of canonical transient receptor potential ion channels in human breast cancer cell lines and tissues: a potential target for breast cancer diagnosis ... in Cancer cell international 2009
Mouse (Murine) Polyclonal TRPC3 Primary Antibody for IHC, IHC (fro) - ABIN259340
Sinai, Ivakine, Lam, Deurloo, Dida, Zirngibl, Jung, Aubin, Feng, Yeomans, McInnes, Osborne, Roder: Disruption of Src Is Associated with Phenotypes Related to Williams-Beuren Syndrome and Altered Cellular Localization of TFII-I(1,2). in eNeuro 2015
Human Polyclonal TRPC3 Primary Antibody for IP, WB - ABIN4362909
Andrikopoulos, Eccles, Yaqoob: Coupling between the TRPC3 ion channel and the NCX1 transporter contributed to VEGF-induced ERK1/2 activation and angiogenesis in human primary endothelial cells. in Cellular signalling 2017
TRPC3contributes to melanoma proliferation and migration through activation of STAT5 (show STAT5A Antibodies)/Akt (show AKT1 Antibodies) signaling.
We also observed that acetylcholine attenuated the formation of NCX1 (show SLC8A1 Antibodies)-TRPC3-IP3R1 (show ITPR1 Antibodies) complexes and maintained calcium homeostasis in cells treated with TNF-alpha (show TNF Antibodies).
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 Antibodies) 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 Antibodies), TRPC3-containing INS (show INS Antibodies) channels are induced by STIM1 (show STIM1 Antibodies), and TRPC1 (show TRPC1 Antibodies)-composed Imax channels are activated by both STIM1 (show STIM1 Antibodies) and STIM2 (show Stim2 Antibodies).
CaSR (show CASR Antibodies) activation mediates Ca2 (show CA2 Antibodies)+ influx and cell proliferation via TRPC3 and TRPC6 (show TRPC6 Antibodies) in human mesangial cells
although gene deletion of TRPC3 or TRPC6 (show TRPC6 Antibodies) alone did not protect against hypertrophy or dysfunction from pressure overload, combined deletion was protective, supporting the value of dual inhibition
TRPC3 deletion prevents mechanical stress-induced ROS production and left ventricular dysfunction in pressure-overloaded heart. TRPC3 specifically contributed to the upregulation of Nox2 in pressure-overloaded heart. TRPC3 participates in pressure overload-induced LV dysfunction in 129 Sv mice.
TRPC3-induced Ca2+ entry promotes astrocyte proliferation and migration i.e. astrocyte activity in vitro which is attenuated by the presence of TRPC1. Following brain injury, the absence of TRPC3 results in a significant reduction of astrogliosis and cortical edema in vivo, suggesting that a targeted therapy to reduce TRPC3 channel activity might be beneficial in traumatic brain injury.
Study shows that the age-dependent alpha-syn accumulation is correlated with an elevation of TRPC3 in the mitochondrial fractions isolated from monkey and mouse brains. In animal and cell models, alpha-syn overexpression was accompanied by an elevation of alpha-syn and TRPC3 in the mitochondrial fractions, and alpha-syn downregulation was associated with a reduction of the mitochondrial alpha-syn and TRPC3.
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 Antibodies) 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 Antibodies)-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 Antibodies) 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 Antibodies)+) influx, but also through control of CaV1.2 (show CACNA1C Antibodies) expressions.
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 Antibodies) protein induce enhanced receptor-activated Ca(2 (show CA2 Antibodies)+) 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