The CHMP4C Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from Raji B lymphocytes, featuring targeted disruption of the CHMP4C gene. This heterogeneous cell pool avoids clonal artifacts and provides a robust loss-of-function model for population-level studies. The Raji line, an EBV+ Burkitt lymphoma, serves as a suspension B-cell platform ideally suited for investigating ESCRT biology and cytokinesis in a lymphoma context.
Raji cells are a well-characterized human B lymphocyte line lacking surface immunoglobulin expression but retaining latent EBV and type III latency gene expression. They are widely employed in immunology and oncology for studies of B-cell signaling, viral transformation, and drug responses. Their rapid proliferation and ease of genetic manipulation make Raji a reliable host for CRISPR-mediated gene disruption, and the absence of endogenous antibody production eliminates interference with downstream immunoassays.
CHMP4C is a core ESCRT-III subunit that executes membrane scission during cytokinetic abscission, multivesicular body (MVB) formation, and viral budding. At the midbody, Aurora B kinase phosphorylates CHMP4C to delay abscission and ensure genomic stability. CHMP4C interacts with ESCRT-III partners CHMP2A and CHMP3, the adaptor ALIX, and the AAA+ ATPases VPS4A/B. It also bridges to the chromosome passenger complex via Borealin, INCENP, and Survivin. Upstream regulators include CDK1/cyclin B, positioning CHMP4C at a nexus of cell division and endosomal sorting.
This knockout model is particularly valuable for studying abscission checkpoint control in EBV-associated lymphoma. Raji cells provide a native environment to examine how viral factors exploit ESCRT machinery for particle release and how CHMP4C loss influences chromosomal instability. Expected phenotypes??multinucleation, abscission delay, and altered MVB ultrastructure??can be directly quantified by microscopy and flow cytometry, linking ESCRT dysfunction to lymphomagenesis.
Applications include mechanistic dissection of ESCRT-dependent cytokinesis, CRISPR-based screening for abscission regulators, evaluation of ESCRT inhibitors in lymphoma, and viral egress studies. Representative assays are Western blot, immunofluorescence for midbody markers, live-cell imaging of cytokinetic progression, flow cytometric DNA content analysis, and electron microscopy of MVBs. For technical assistance or custom applications, please contact Ascent Research.
