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Transient receptor potential cation channel, subfamily C, member 3

TRPC3, Trp3
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. [provided by RefSeq, Oct 2011] (from NCBI)
Top mentioned proteins: Trp6, TRPC1, CAN, TRPC4, V1a
Papers using TRPC3 antibodies
The role of TRPV6 in breast carcinogenesis
Palmer Christopher et al., In Cancer Cell International, 2007
... A mouse anti-TRPC3 polyclonal antibody was obtained from the Abnova Corporation and used at ...
Papers on TRPC3
Ca(2+) Signalling in Endothelial Progenitor Cells: Friend or Foe?
Guerra et al., Pavia, Italy. In J Cell Physiol, Feb 2016
However, the Ca(2+) machinery underlying VEGF-induced Ca(2+) spikes changes in umbilical cord blood-derived EPCs, which require TRPC3-mediated Ca(2+) entry to trigger the interplay between InsP3 and SOCE.
Critical roles of Gi/o proteins and phospholipase C-δ1 in the activation of receptor-operated TRPC4 channels.
Zhu et al., Homburg, Germany. In Proc Natl Acad Sci U S A, Feb 2016
Although TRPC3/C6/C7 can be directly activated by diacylglycerols produced by PLC breakdown of phosphatidylinositol 4,5-bisphosphate (PIP2), the mechanism by which the PLC pathway activates TRPC4/C5 remains unclear.
Screening of TRPC Channel Activators Identifies Novel Neurotrophic Piperazine Compounds.
Mori et al., Kyoto, Japan. In Mol Pharmacol, Feb 2016
Among the TRPC subfamily, TRPC3 and TRPC6 channels activated directly by diacylglycerol (DAG) play important roles in brain-derived neurotrophic factor (BDNF) signaling, promoting neuronal development and survival.
Mibefradil suppresses the proliferation of pulmonary artery smooth muscle cells.
Shen et al., Shanghai, China. In J Investig Med, Jan 2016
however, no changes in TRPC1, TRPC3, CAV1.2, and CAV3.2 levels were observed.
Intracellular spermine blocks TRPC4 channel via electrostatic interaction with C-terminal negative amino acids.
So et al., Seoul, South Korea. In Pflugers Arch, Jan 2016
The inhibition was specific to TRPC4 and TRPC5 channels but was not effective to TRPC1/4, TRPC1/5, and TRPC3 channels.
TRPC3-dependent synaptic transmission in central mammalian neurons.
Konnerth et al., München, Germany. In J Mol Med (berl), Sep 2015
TRPC3, one of the seven members of the TRPC subfamily, combines functions of an unspecific ion channel and a signal transducer.
Decreased levels of canonical transient receptor potential channel 3 protein in the rat cerebral cortex after chronic treatment with lithium or valproate.
Emamghoreishi et al., Shīrāz, Iran. In Res Pharm Sci, Sep 2015
TRPC3 and TRPM2, are potential candidates involved in calcium signaling and implicated in the pathophysiology of bipolar disorder.
Brain transient receptor potential channels and stroke.
Liao et al., Singapore, Singapore. In J Neurosci Res, Aug 2015
In stroke, TRPC3/4/6, TRPM2/4/7, and TRPV1/3/4 channels have been found to participate in ischemia-induced cell death, whereas other TRP channels, in particular those expressed in nonneuronal cells, have been less well studied.
Psychiatric Disorders and TRP Channels: Focus on Psychotropic Drugs.
Demirdaş et al., Isparta, Turkey. In Curr Neuropharmacol, 2014
Intracellular calcium influx induced by oxidative stress has an significant role in the etiology of bipolar disorders (BDs), and studies recently reported the important role of TRP channels such as TRPC3, TRPM2, and TRPV1 in converting oxidant or nitrogen radical signaling to cytosolic calcium ion homeostasis in BDs.
TRPs in hearing.
Göpfert et al., Göttingen, Germany. In Handb Exp Pharmacol, 2013
In vertebrates, TRPs are unlikely to form auditory transduction channels, yet most TRPs are expressed in inner ear tissues, and mutations in TRPN1, TRPVA1, TRPML3, TRPV4, and TRPC3/TRPC6 have been implicated in inner ear function.
Alternative splicing of the TRPC3 ion channel calmodulin/IP3 receptor-binding domain in the hindbrain enhances cation flux.
Housley et al., Sydney, Australia. In J Neurosci, 2012
This study demonistrated that Alternative splicing of the TRPC3 ion channel has enhanced efficacy as a neuronal GPCR-Ca(2+) signaling effector, and is associated with sensorimotor coordination, neuronal development, and brain injury.
Transient receptor potential canonical 3 (TRPC3) is required for IgG immune complex-induced excitation of the rat dorsal root ganglion neurons.
Ma et al., New Haven, United States. In J Neurosci, 2012
Transient receptor potential canonical 3 (TRPC3) is required for IgG immune complex-induced excitation of the rat dorsal root ganglion neurons.
Williams-Beuren syndrome hypercalcemia: is TRPC3 a novel mediator in calcium homeostasis?
Haymann et al., Paris, France. In Pediatrics, 2012
Calcium metabolism abnormalities observed in Williams-Beuren syndrome may be attributable to transcription factor IIi gene haploinsufficiency and subsequent TRPC3 overexpression.
Pulsatile atheroprone shear stress affects the expression of transient receptor potential channels in human endothelial cells.
Tepel et al., Berlin, Germany. In Hypertension, 2012
Data show the expression of TRPC6 and TRPV1 was significantly increased after 24 hours of exposure to an atheroprone flow, whereas the expression of TRPC3 and TRPM7 was significantly higher in endothelial cells exposed to shear stress.
Increased migration of monocytes in essential hypertension is associated with increased transient receptor potential channel canonical type 3 channels.
Tepel et al., Chongqing, China. In Plos One, 2011
In the presence of 2-APB or after siRNA knockdown of TRPC3 the fMLP-induced monocyte migration was significantly blocked in hypertensive patients compared to normotensive control subjects.
STIM1 heteromultimerizes TRPC channels to determine their function as store-operated channels.
Muallem et al., Dallas, United States. In Nat Cell Biol, 2007
Through a distinct mechanism, STIM1 also regulates TRPC3 and TRPC6.
Action of TFII-I outside the nucleus as an inhibitor of agonist-induced calcium entry.
Desiderio et al., Baltimore, United States. In Science, 2006
observations suggest a model in which TFII-I suppresses agonist-induced calcium entry by competing with TRPC3 for binding to phospholipase C-gamma
STIM1 carboxyl-terminus activates native SOC, I(crac) and TRPC1 channels.
Worley et al., Baltimore, United States. In Nat Cell Biol, 2006
Activity of STIM1 requires an ERM domain, which mediates the selective binding of STIM1 to TRPC1, 2 and 4, but not to TRPC3, 6 or 7, and a cationic lysine-rich region, which is essential for gating of TRPC1.
Essential role of TRPC channels in the guidance of nerve growth cones by brain-derived neurotrophic factor.
Yuan et al., Shanghai, China. In Nature, 2005
Several members of the TRPC family are highly expressed in these neurons, and both Ca2+ elevation and growth-cone turning induced by BDNF are abolished by pharmacological inhibition of TRPC channels, overexpression of a dominant-negative form of TRPC3 or TRPC6, or downregulation of TRPC3 expression via short interfering RNA.
Pleckstrin homology domains: two halves make a hole?
Lemmon, Philadelphia, United States. In Cell, 2005
In a recent issue of Nature, van Rossum et al. report binding of a "split" pleckstrin homology (PH) domain from phospholipase C-gamma(1) to the TRPC3 ion channel.
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