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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)
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
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.
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