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CHO-K1/Human CXCR7(ACKR3) β-Arrestin Stable Cell

Item
Cat#
Price

Stable Cell Line

SNB-A-0072D

Inquiry

Compound Testing Services

CT-001

$1,850 per 384w plate

(Up To 16 cpds Dose)


Product Description


CXCR7 (ACKR3) is a class A GPCR that acts as a scavenger receptor by recruiting β‑arrestin to internalize and degrade its ligands CXCL12 and CXCL11, thereby regulating chemokine gradients. It is expressed in placenta, brain endothelium, heart, adrenal gland, embryonic tissues, and upregulated in activated endothelial cells and tumors. Activation promotes ligand clearance and β‑arrestin‑dependent MAPK signaling, affecting cell migration, proliferation, and survival.

 

ScreeningBio’s human CXCR7(ACKR3) β-arrestin cell line is an ideal tool for studying GPCR/β-arrestin interactions. In this system, the GPCR C-terminus is fused to a smallBiT tag, and the β2-arrestin N-terminus is fused to a largeBiT tag. Upon receptor activation, GPCR/β-arrestin interaction brings the two fragments together to reconstitute an active NanoLuc enzyme, which can be quantified using the NanoBiT substrate. This cell line is designed to evaluate a compound’s ability to activate the β-arrestin signaling pathway. 

Product Specifications

Target Type

GPCR

Species

Human

HGNC Symbol

ACKR3

Accession Number

NM_020311 (Hs)

Parental Line

CHO-K1

Lot#

See Vial

Storage

Liquid Nitrogen


Data


CHO-K1/Human CXCR7(ACKR3) β-Arrestin Agonist Assay. CHO-K1/Human CXCR7(ACKR3) β-Arrestin cells were treated with the reference agonist. Non-linear regression was used to plot activity changes vs. [Compound, M], and EC50 /IC50 values were determined, using GraphPad Prism software.
CHO-K1/Human CXCR7(ACKR3) β-Arrestin Agonist Assay. CHO-K1/Human CXCR7(ACKR3) β-Arrestin cells were treated with the reference agonist. Non-linear regression was used to plot activity changes vs. [Compound, M], and EC50 /IC50 values were determined, using GraphPad Prism software.


Target Background


CXCR7 (ACKR3) is a class A GPCR that acts as a scavenger receptor by recruiting β‑arrestin to internalize and degrade its ligands CXCL12 and CXCL11, thereby regulating chemokine gradients.


It is expressed in placenta, brain endothelium, heart, adrenal gland, embryonic tissues, and upregulated in activated endothelial cells and tumors. Activation promotes ligand clearance and β‑arrestin‑dependent MAPK signaling, affecting cell migration, proliferation, and survival.

 



Product Documentation



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