The CHMP2B Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-mediated polyclonal knockout cell population derived from the Raji human B lymphocyte cell line. This product disrupts the CHMP2B gene, encoding a critical subunit of the endosomal sorting complexes required for transport (ESCRT)-III complex. The resulting loss-of-function model provides a powerful tool for dissecting CHMP2B-dependent membrane remodeling processes without clonal selection artifacts. These polyclonal knockout cells are suitable for functional genomics, endosomal trafficking studies, and autophagy research.
Raji is a Burkitt lymphoma-derived B lymphocyte cell line widely employed in immunology and cancer biology. As a B lymphocyte model, Raji cells are committed to antibody production and adaptive immune responses, making them valuable for studying B-cell signaling, lymphomagenesis, and vesicular transport pathways. Their robust growth and well-characterized endomembrane system facilitate investigation of multivesicular body (MVB) formation, exosome secretion, and lysosomal degradation. The CHMP2B knockout in this background allows assessment of ESCRT-III function specifically within the context of B-cell physiology and lymphoma-associated trafficking dysregulation.
CHMP2B functions as a core ESCRT-III subunit that polymerizes to drive membrane scission during intralumenal vesicle formation and autophagosome closure. Upstream regulators include the ESCRT-II complex, VPS4, IST1, and ubiquitin, which control CHMP2B assembly and disassembly. CHMP2B directly interacts with ESCRT-III partners CHMP2A and CHMP4B, as well as accessory factors ALIX, TSG101, and IST1. Downstream targets encompass the EGF receptor, autophagic substrates, and MVB cargoes destined for lysosomal degradation or extracellular release. Through these interactions, CHMP2B orchestrates endosomal sorting, autophagy, and lysosomal clearance, linking it to pathways that maintain cellular proteostasis and modulate receptor signaling.
In Raji cells, CHMP2B knockout disrupts endosomal sorting and lysosomal degradation, impairing proteostasis and altering signaling dynamics. This dysfunction perturbs exosome biogenesis and autophagic flux, processes essential for B-cell homeostasis and response to extracellular cues. Because CHMP2B is implicated in frontotemporal dementia and amyotrophic lateral sclerosis, this model enables investigation of neurodegeneration mechanisms in a tractable cellular system. Moreover, the Raji background provides a unique platform to explore ESCRT-III contributions to lymphomagenesis, antigen presentation, and adaptive immunity, given the cell line’s B lymphocyte origin.
Researchers can utilize these polyclonal knockout cells in diverse applications, including endosomal trafficking studies, autophagy research, neurodegeneration modeling, cancer cell biology, and exosome characterization. Representative assays such as western blotting, immunofluorescence, flow cytometry, autophagy flux assays, co-immunoprecipitation, and electron microscopy allow detailed analysis of CHMP2B-dependent processes. For example, monitoring EGFR degradation kinetics, quantifying autophagosome accumulation, or examining MVB ultrastructure under knockout conditions provides mechanistic insight into CHMP2B function. This flexible system supports drug screening and genetic rescue experiments. For further details, please contact Ascent Research.
