Our Anti-TrpC4 mouse monoclonal primary antibody from NeuroMab is produced in-house from hybridoma clone N77/15. It detects human, mouse, and rat TrpC4, and is purified by Protein A chromatography. It is great for use in IHC, ICC, IP, WB.
Adult rat brain membrane (RBM) and transfected cell immunoblot: extracts of RBM and COS cells transiently transfected with TrpC4 and probed with N77/15 TC supe.
Short transient receptor potential channel 4 or TrpC4 is encoded by the gene TrpC4. TrpC4 belongs to the transient receptor family, a group of membrane bound ion channels that have a relatively non-selective permeability to cations, including sodium, calcium and magnesium. This protein is thought to have a role as a cell-cell contact-dependent endothelial calcium entry channel. Trpc4 is found in many tissues including CNS, placenta, heart, smooth muscle, testis, kidney and brain. Mutations in this gene areassociated with generalized epilepsy with photosensitivity.
Purified by Protein A chromatography
1 mg/mL
Monoclonal
N77/15
IgG2b
ICC, IHC, IP, WB
Mouse
Trpc4
110 kDa
Synthetic peptide amino acids 930-947 (FKSEKVVVEDTVPIIPKE) of rat TrpC4 (accession number O35119)
Human, Mouse, Rat
AB_2256454
Aliquot and store at ≤ -20°C for long term storage. For short term storage, store at 2-8°C. For maximum recovery of product, centrifuge the vial prior to removing the cap.
Liquid
Produced by in vitro bioreactor culture of hybridoma line followed by Protein A affinity chromatography. Purified mAbs are >90% specific antibody.
10 mM Tris, 50 mM Sodium Chloride, 0.065% Sodium Azide pH 7.46
Unconjugated
No cross-reactivity reported
Each new lot of antibody is quality control tested on cells overexpressing target protein and confirmed to give the expected staining pattern.
These antibodies are to be used as research laboratory reagents and are not for use as diagnostic or therapeutic reagents in humans.
Riccio, A., et al. 2014. Decreased anxiety-like behavior and Gαq/11-dependent responses in the amygdala of mice lacking TRPC4 channels.. Journal of Neuroscience, 3653-3667.
Inoue, M., et al. 2012. Mechanisms and roles of muscarinic activation in guinea-pig adrenal medullary cells.. American Journal of Physiology-Cell Physiology, C635-644.
Kollewe, A., et al. 2022. Subunit Composition, Molecular Environment, and Activation of Native TRPC Channels Encoded by Their Interactomes. Neuron, 4162-4175.
Amores-Bonet, L., et al. 2022. Interactions between the Polysialylated Neural Cell Adhesion Molecule and the Transient Receptor Potential Canonical Channels 1, 4, and 5 Induce Entry of Ca2+ into Neurons. International Journal of Molecular Science, 10027.
Soni, H., et al. 2017. Urotensin II-induced store-operated Ca2+ entry contributes to glomerular mesangial cell proliferation and extracellular matrix protein production under high glucose conditions. Scientific Reports, 18049.
Riccio, A., et al. 2014. Decreased anxiety-like behavior and Gαq/11-dependent responses in the amygdala of mice lacking TRPC4 channels.. Journal of Neuroscience, 3653-3667.
Abou-Saleh, H., et al. 2013. Inositol 1,4,5-trisphosphate (IP3) receptor up-regulation in hypertension is associated with sensitization of Ca2+ release and vascular smooth muscle contractility.. The Journal of Biological Chemistry, 32941-32951.
Jeon, J.P., et al. 2012. Selective Gαi subunits as novel direct activators of transient receptor potential canonical (TRPC)4 and TRPC5 channels.. The Journal of Biological Chemistry, 17029-17039.
Wang, L.K., et al. 2017. Elevated Expression of TRPC4 in Cortical Lesions of Focal Cortical Dysplasia II and Tuberous Sclerosis Complex. Journal of Molecular Neuroscience, 222-231.
Klipec, W.D., et al. 2016. Loss of the trpc4 gene is associated with a reduction in cocaine self-administration and reduced spontaneous ventral tegmental area dopamine neuronal activity, without deficits in learning for natural rewards. BehaviorBrain Research, 117-127.
Lee, J.E., et al. 2012. Mass spectrometric analysis of novel phosphorylation sites in the TRPC4β channel.. Rapid Communications in Mass Spectrometry, 1965-1970.
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