The ART1 Knockout AGS Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population generated from the AGS human gastric adenocarcinoma cell line, featuring targeted disruption of the ART1 gene. This heterogeneous cell pool provides a robust loss-of-function system for investigating ART1-dependent signaling in a gastric epithelial context, without the biases of single?cell clonal selection. The polyclonal format is particularly suited to pooled screening approaches and population?level functional assays, enabling researchers to interrogate gene function across a spectrum of mutational events.
The AGS cell line is a widely used human gastric adenocarcinoma model originally established from a primary tumor of a 54?year?old male patient. These cells recapitulate key features of the gastric epithelium and serve as a platform for studying gastric cancer biology, host?pathogen interactions, and epithelial?immune crosstalk. Their adherent growth and well?characterized signaling pathways make them a reliable choice for in vitro experiments aimed at dissecting molecular mechanisms of gastric carcinogenesis and inflammation.
ART1 encodes an ADP?ribosyltransferase that specifically catalyses the transfer of ADP?ribose from NAD? to arginine residues on target proteins, most notably the P2X7 purinergic receptor. ART1 expression is transcriptionally regulated by inflammatory stimuli via the NF???B and STAT1 pathways downstream of cytokines such as IFN??? and TNF???. ART1?mediated ADP?ribosylation of P2X7 modulates its activity and downstream signaling, including activation of the NLRP3 inflammasome. The ADP?ribosylated P2X7 assembles with ASC and caspase?1 to promote cleavage and release of mature IL?1??. ART1 also interacts with GPI?anchor components and localizes to lipid rafts, positioning it as a critical node in purinergic?to?inflammatory signal transduction within gastric epithelial cells.
In gastric adenocarcinoma, ART1?driven ADP?ribosylation can influence tumor?associated inflammation, immune evasion, and cell fate decisions. Disrupting ART1 in AGS cells therefore provides a valuable model to dissect how this post?translational modification shapes the epithelial response to purinergic danger signals and inflammatory cytokines. This knockout system allows the examination of ART1??s contribution to canonical NF???B activation, inflammasome assembly, and downstream cytokine production, all pathways implicated in gastric cancer progression and maintenance of a tumor?permissive microenvironment.
The ART1 Knockout AGS Polyclonal Cells are suited for a wide range of experimental applications, including Western blotting for ADP?ribosylated proteins, ELISA for IL?1?? secretion, quantitative RT?PCR for inflammasome components, flow cytometry for P2X7 surface expression, and co?immunoprecipitation studies to probe ART1?P2X7 interactions. They may also be employed in inflammasome activation assays, cell viability and migration/invasion studies, and drug screening aimed at identifying modulators of ADP?ribosylation signaling in a gastric cancer context. For further information, please contact Ascent Research.
