The DTX3L Knockout AGS Polyclonal Cells represent a CRISPR/Cas9-edited human polyclonal knockout cell population designed for loss-of-function studies of DTX3L. This product provides a heterogeneous gene-disrupted model generated in the AGS gastric adenocarcinoma cell line, enabling investigation of DTX3L-dependent mechanisms without clonal selection artifacts. The polyclonal format preserves the genetic diversity of the edited pool, supporting robust functional assays and target validation studies.
The parental AGS cell line is a widely characterized epithelial model derived from a human gastric adenocarcinoma. AGS cells are extensively employed in stomach cancer research, including studies of tumorigenesis, drug sensitivity, and host?Cpathogen interactions such as Helicobacter pylori infection. Their adherent growth and well-documented signaling characteristics make them a reliable platform for CRISPR/Cas9-mediated genetic perturbation.
DTX3L encodes an E3 ubiquitin-protein ligase that, in complex with PARP9, catalyzes the ubiquitination of histone H2A/H2B and signaling adaptors. This activity enhances STAT1 phosphorylation and transcriptional activation downstream of interferon receptors (IFNAR1) and associated kinases JAK1 and TYK2, thereby promoting interferon-stimulated gene expression. DTX3L also facilitates NF-??B signaling through interaction with NFKB1 and RELA, integrating innate immune responses and DNA damage repair via ubiquitin-mediated proteolysis.
In gastric cancer, DTX3L may influence cell proliferation, apoptosis, and chemoresistance by modulating interferon and NF-??B pathways. The DTX3L knockout in AGS cells provides a physiologically relevant model to dissect how ubiquitination-dependent immune signaling contributes to gastric cancer progression and treatment sensitivity. This system is especially suited for exploring the crosstalk between inflammatory signals and oncogenic networks in an epithelial tumor context.
Researchers can apply this knockout model in diverse assays including Western blotting, RT?qPCR, RNA?seq, co?immunoprecipitation, and ubiquitination assays to characterize DTX3L interactors and downstream targets. Functional studies may employ NF???B reporter assays, interferon?stimulated gene expression analysis, and cell-based viability (MTT) or apoptosis (Annexin V/PI) readouts. Migration/invasion (Transwell) and drug sensitivity testing (e.g., cisplatin) further enable investigation of metastatic potential and therapeutic resistance. For further details or to discuss custom applications, please contact Ascent Research.
