MULTISCREEN™ STABLE CELL LINES

HUMAN RECOMBINANT GPR17 RECEPTOR

Product Information

Catalog Number:
C1076-3

Lot Number:
C1076-3-090814

Quantity:
1 vial (2 x 106) frozen cells

Freeze Medium:
Sigma Freezing Medium (C-6164)

Host cell:
1321N1

Transfection:
Expression vector containing full-length human GPR17cDNA (GenBank Accession Number NM_005291) with FLAG tag sequence at N-terminus

Recommended Storage:
Liquid nitrogen upon receiving

Propagation Medium: DMEM, 10% FBS, 1 μg/mL puromycin

Stability:
Stable in culture for minimum of two months

Data Sheet

Background: G-protein coupled receptor 17 (GPR17) is closely related to the purinergic and cysteinyl-leukotriene receptor families. It is present on both neurons and a subset of oligiodendrocyte precursor cells. Recent studies have shown that GPR17 plays an important role in both sensing and repairing brain damage. Thus, GPR17 represents a potential new target for the treatment of traumatic brain injuries as well as neurodegenerative diseases like Alzheimer’s and multiple sclerosis.

Application: Functional assays

Figure 1. Dose-dependent inhibition of forskolin-stimulated intracellular cAMP level upon treatment with ligand, measured with MultiscreenTM TR-FRET cAMP 1.0 No Wash Assay Kit (Multispan MSCM01). Figure 2. Receptor expression on cell surface measured by flow cytometry (FACS) using an anti-FLAG antibody. Thin line: parental cells; thick line: receptor- expressing cells.

References:

Franke, Heike et al. “Changes of the GPR17 Receptor, a New Target for Neurorepair, in Neurons and Glial Cells in Patients with Traumatic Brain Injury.”Purinergic Signalling 9.3 (2013): 451–462. PMC. Web. 18 Feb. 2015.

Hennen, S et al. “Decoding Signaling and Function of the Orphan G Protein-Coupled Receptor GPR17 with a Small-Molecule Agonist.”Sci Signal 2013 Oct 22;6(298)
 
Lecca, Davide et al. “The Recently Identified P2Y-Like Receptor GPR17 Is a Sensor of Brain Damage and a New Target for Brain Repair.” Ed. Kenji Hashimoto. PLoS ONE 3.10 (2008): e3579. PMC. Web. 18 Feb. 2015
 

 

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