The CHMP1B Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human AGS gastric adenocarcinoma cell line, engineered to disrupt the CHMP1B gene. This product provides a heterogeneous pool of cells with targeted disruption of CHMP1B, enabling the study of loss-of-function phenotypes in a gastric cancer model. The polyclonal format preserves biological variability while ensuring robust knockout, making it suitable for functional investigations where clonal artifacts are undesirable.
The host AGS cell line was established from the gastric adenocarcinoma of a 54-year-old female patient and is widely employed as a model system for gastric cancer research. These adherent epithelial cells exhibit characteristics of invasive gastric carcinoma and are responsive to various growth factors and chemotherapeutic agents. The AGS background provides a clinically relevant platform to examine oncogenic signaling, tumor progression, and drug resistance pathways.
CHMP1B encodes a core component of the ESCRT-III complex, which polymerizes into filaments that drive membrane scission during essential cellular processes, including multivesicular body (MVB) formation, cytokinetic abscission, and viral budding. CHMP1B functions downstream of EGF receptor signaling and ubiquitinated cargo recognition by the ESCRT-0/HRS complex and ALIX. It interacts directly with ESCRT-III partners CHMP2A and CHMP3, the AAA-ATPase VPS4, and regulatory factors IST1 and Vta1 to execute membrane remodeling. Disruption of CHMP1B impairs the ESCRT pathway, leading to defective EGFR degradation, altered exosome secretion, and failure of receptor tyrosine kinase downregulation, thereby affecting key signaling cascades.
In the context of gastric adenocarcinoma, CHMP1B knockout creates a unique loss-of-function model to dissect the role of endosomal sorting in cancer biology. Impaired ESCRT-III activity can result in sustained surface expression and signaling of growth factor receptors such as EGFR, potentially driving proliferation, invasion, and metastasis. This model is thus highly relevant for investigating mechanisms of drug resistance, epithelial-to-mesenchymal transition, and exosome-mediated tumor microenvironment communication. Additionally, CHMP1B dysfunction has been implicated in neurodegenerative diseases like frontotemporal dementia and amyotrophic lateral sclerosis, as well as in host responses to viral infections, broadening the model’s translational scope.
Researchers can employ this knockout cell pool in a range of functional studies, including endosomal trafficking analyses via immunofluorescence for ESCRT markers and ultrastructural examination of MVBs by transmission electron microscopy. Western blotting of components such as TSG101, CHMP2A, and VPS4 can validate pathway perturbation, while flow cytometry enables kinetic assays of receptor turnover (e.g., EGFR). Functional assays such as wound healing and Transwell invasion quantify migratory and invasive behavior, and exosome isolation coupled with characterization facilitates intercellular communication studies. This versatile tool supports investigations into ESCRT-mediated processes, cancer cell signaling, and host?Cviral interactions. For further details, please contact Ascent Research.
