This product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line, designed to disrupt the IL1B gene locus. The polyclonal format provides a heterogeneous pool of cells carrying gene-editing events across the target gene, generating a loss-of-function model without the selection of a single clonal isolate. This knockout approach enables investigation of IL1B-dependent signaling and functional outcomes in a physiologically relevant gastric epithelial context, while maintaining the inherent biological variability of the parental cell line. The product is suitable for applications requiring abrogation of interleukin-1?? expression and subsequent downstream signaling analysis.
The AGS cell line originates from a human gastric adenocarcinoma and serves as a widely employed model for studying gastric epithelial cell biology, host?Cpathogen interactions, and gastric carcinogenesis. These adherent cells retain epithelial characteristics and are responsive to microbial virulence factors such as those from Helicobacter pylori. AGS cells express critical signaling molecules involved in innate immune responses, making them an appropriate platform for dissecting cytokine-mediated inflammation and transformation pathways relevant to gastric disease.
IL1B encodes interleukin-1?? (IL-1??), a potent pro-inflammatory cytokine that is synthesized as an inactive precursor and processed by caspase-1, typically within the NLRP3 inflammasome complex. Upon secretion, IL-1?? binds to the IL-1 receptor type I (IL1R1) and recruits the IL-1 receptor accessory protein (IL1RAP), triggering MYD88-dependent signal transduction. This cascade recruits IRAK4 and TRAF6, leading to activation of TAK1 and subsequent stimulation of the IKK??/?¨CNF-??B and p38 MAPK?CJNK?CAP-1 pathways. Key downstream targets transcriptionally regulated by these pathways include IL-6, CXCL8 (IL-8), PTGS2 (COX-2), MMP-9, ICAM-1, and CCL2 (MCP-1). Upstream regulators that induce IL1B expression in AGS cells encompass TNF-??, bacterial lipopolysaccharide, Toll-like receptor agonists, NLRP3 inflammasome activation, NF-??B, and AP-1 transcription factors. Interacting proteins critical for IL-1?? signaling and activation include IL1RAP, IL1RN, caspase-1, NLRP3, and the adaptor ASC (PYCARD).
In the gastric epithelial context, IL-1?? is a central mediator of Helicobacter pylori-induced chronic inflammation and a contributor to gastric carcinogenesis. H. pylori virulence factors, such as CagA, stimulate IL1B expression, leading to autocrine and paracrine signaling that promotes pro-inflammatory cytokine production, epithelial cell survival, and tissue remodeling. The resulting inflammatory microenvironment can drive progression from chronic gastritis to atrophy, metaplasia, and adenocarcinoma. By disrupting IL1B in AGS cells, this polyclonal knockout model permits rigorous dissection of IL-1??-dependent signaling modules and their roles in infection-driven inflammation and malignant transformation.
This knockout cell population is suited for a wide range of experimental applications, including mechanistic studies of IL-1?? signaling in gastric cancer, functional analysis of the NLRP3 inflammasome in epithelial cells, and H. pylori infection models to delineate host-response networks. Typical assays include ELISA quantification of secreted cytokines, RT-qPCR for downstream target gene expression, Western blot analysis of NF-??B and MAPK phosphorylation, immunofluorescence detection of NF-??B nuclear translocation, scratch wound healing and transwell invasion assays to assess cell migration, and cell proliferation assays such as MTT or CCK-8. The polyclonal nature also supports pooled CRISPR screening and drug sensitivity profiling for anti-inflammatory or anti-cancer agents targeting IL-1??-dependent pathways. For further technical details, please contact Ascent Research.
