TRPM2-HEK293 Recombinant Cell Line

Catalog #
90331
$10,340 *
Size: 2 vials
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Description

Stable, recombinant HEK293 cell line expressing tetracycline-inducible human TRPM2 (transient receptor potential cation channel, subfamily M, member 2, accession number NM_003307).

This product has been cited 1 time.

Purchase of this cell line is for research purposes only; commercial use requires a separate license. View the full terms and conditions.

Synonyms
transient receptor potential cation channel, subfamily M, member 2, TRPM2, KNP3, previously TRPC7
Product Info
Storage and Usage
Citations1
Host Cell Line
HEK293 cells
Species
Human
Supplied As
Each vial contains ~1.5 X 106 cells in 1 ml of 10% DMSO.
Biological Activity
N-terminal FLAG tagged human TRPM2 channel has been stably integrated into HEK293 cells and its expression can be induced by tetracycline (doxycycline). The tetracycline-inducible expression of TRPM2 was confirmed by Western blotting. The function of TRPM2 was characterized by calcium assay. TRPM2-HEK293 cells were pre-treated with doxycycline to induce the expression of TRPM2, then stimulated with H2O2, and calcium influx was observed. The H2O2-induced calcium influx via TRPM2 could be blocked by N-(p-Amylcinnamoyl) anthranilic Acid (ACA), a TRP channel blocker.
Genbank #
NM_003307
UniProt #
O94759
Mycoplasma Testing
The cell line has been screened using the PCR-based VenorGeM Mycoplasma Detection kit (Sigma Aldrich) to confirm the absence of Mycoplasma species.
Background
TRPM2 channel belongs to the transient receptor potential channel (TRP) superfamily which is divided into seven main subfamilies. TRPM2 channel is a nonselective, calcium-permeable cation channel highly expressed in the brain, vascular smooth muscle, endothelial cells and immune cells. It is activated by oxidative stressors such as hydrogen peroxide, cyclic ADP ribose, and NADP, leading to an increase in the intracellular free calcium concentration and cell death. TRPM2 is a potential drug target in a variety of human diseases, including cardiovascular and neurodegenerative diseases.
References
1. Moran, M.M., et al. (2011). Nat. Rev. Drug Discov. 10(8):601-620
2. Song, Y., et al. (2008) J. Biomol. Screen. 13(1):54-61
3. Fonfria, E., et al. (2004). Br. J. Pharmacol. 143(1):186-192.