The GPR171 Knockout AGS Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout population of AGS human gastric epithelial cells with targeted disruption of the GPR171 gene. This loss-of-function model, generated via CRISPR-mediated gene ablation, provides a heterogeneous cell pool lacking GPR171 expression, enabling robust functional studies while avoiding clonal selection biases.
AGS cells, derived from a human gastric adenocarcinoma, serve as a standard epithelial model for gastric cancer and Helicobacter pylori infection research. The cell line??s adherent morphology and well-characterized signaling properties make it ideal for investigating tumor cell biology, drug responses, and host?Cpathogen interactions.
GPR171 is an orphan GPCR activated by BigLEN, a peptide derived from proSAAS. It couples through G??i/o proteins to inhibit adenylyl cyclase, decreasing cAMP and attenuating PKA-CREB signaling. ??-arrestin2 recruitment mediates ERK1/2 phosphorylation, engaging the MAPK pathway. Additionally, GPR171 modulates NF-??B in response to inflammatory cytokines such as TNF?? and IL-1??, linking it to immune modulation and positioning the receptor at the intersection of chemokine-like signaling, cAMP dynamics, and immune cell function.
In the context of gastric adenocarcinoma, GPR171 knockout AGS cells provide a unique model to dissect the receptor’s contributions to tumor-intrinsic signaling and the tumor immune microenvironment. Loss of GPR171 enables evaluation of altered cytokine secretion, immune cell recruitment, and tumor cell proliferation, key processes in gastric cancer progression and immunoediting.
Functional assays include cAMP measurement, phospho-ERK western blotting, and NF-??B reporter analysis for signaling validation; MTT proliferation, wound-healing migration, and transwell invasion tests for cellular phenotype; and cytokine profiling for immune response assessment. Co-culture systems with immune cells and RNA-seq facilitate studies of tumor?Cimmune crosstalk and transcriptomic changes. This polyclonal knockout model supports drug target validation and mechanistic investigations of chemokine and GPCR signaling in gastric cancer. For further information, please contact Ascent Research.
