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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. Zusätzlich bieten wir Ihnen TRPC3 Antikörper (85) und viele weitere Produktgruppen zu diesem Protein an.
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Diacylglycerol generation downstream of VEGF receptors activatesTRPC3 causing Na(+) influx with subsequent reversal of NCX1, ERK1/2 activation and ultimately contributes to enhanced angiogenesis.
TRPC3contributes to melanoma proliferation and migration through activation of STAT5 (zeige STAT5A Proteine)/Akt (zeige AKT1 Proteine) signaling.
We also observed that acetylcholine attenuated the formation of NCX1 (zeige SLC8A1 Proteine)-TRPC3-IP3R1 (zeige ITPR1 Proteine) complexes and maintained calcium homeostasis in cells treated with TNF-alpha (zeige TNF Proteine).
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 (zeige TRPC6 Proteine) 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 (zeige Stim2 Proteine), TRPC3-containing INS (zeige INS Proteine) channels are induced by STIM1 (zeige STIM1 Proteine), and TRPC1 (zeige TRPC1 Proteine)-composed Imax channels are activated by both STIM1 (zeige STIM1 Proteine) and STIM2 (zeige Stim2 Proteine).
CaSR (zeige CASR Proteine) activation mediates Ca2 (zeige CA2 Proteine)+ influx and cell proliferation via TRPC3 and TRPC6 (zeige TRPC6 Proteine) in human mesangial cells
Sarcolemmal TRPC3, regulated by AT1R (zeige AGTRAP Proteine), causes the SSC (zeige CYP11A1 Proteine).
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.
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 (zeige TRPC6 Proteine) 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 (zeige FGFR3 Proteine)-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
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 (zeige TRPM2 Proteine) protein induce enhanced receptor-activated Ca(2 (zeige CA2 Proteine)+) 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