This Raji polyclonal cell product features CRISPR/Cas9-mediated disruption of the CCM2 gene, generating a loss-of-function pool for studying CCM2 biology in human B lymphocytes. The polyclonal knockout population preserves genetic heterogeneity while abrogating CCM2 protein expression, suited for robust biochemical and phenotypic analyses without clonal selection artifacts. This format is ideal for applications requiring representative cellular diversity, such as signaling studies and drug testing.
The Raji host cell line is a human Epstein-Barr virus-immortalized B lymphoblastoid line derived from a Burkitt lymphoma. Raji cells are suspension-adapted, express surface integrins and immunoglobulin, and provide a well-characterized model for B cell biology, antibody production, and lymphomagenesis. Their stable genetic background and ease of culture make them suitable for knockout studies. CCM2 disruption in this hematopoietic context allows dissection of its role in lymphocyte adhesion, migration, and signal transduction, distinct from its canonical endothelial function.
CCM2 is a scaffold protein that, together with KRIT1 and PDCD10, forms the CCM complex to suppress RhoA-ROCK signaling. It interacts with integrin ??1, ITGB1BP1, and HEK1, linking cell adhesion receptors to actin cytoskeleton regulation. Upstream inputs from integrins, VEGFR, and mechanical cues modulate complex assembly. Loss of CCM2 disinhibits RhoA, leading to ROCK-mediated phosphorylation of MLC and MYPT1, and increased stress fiber formation, thereby compromising cell adhesion. This dysregulation is central to the pathogenesis of cerebral cavernous malformations but may also influence hematopoietic cell behavior.
In Raji B cells, CCM2 knockout provides a novel model to explore its non-endothelial functions. B lymphocytes depend on integrin-mediated adhesion and actin dynamics for immune function and lymphoma dissemination. Unchecked RhoA-ROCK signaling in CCM2-deficient Raji cells may alter integrin surface profiles, enhance contractility, and impair adhesion and migration, mirroring aspects of aggressive lymphoma. This polyclonal system facilitates the study of CCM2??s role in B cell malignancies and the evaluation of CCM complex-targeting therapies.
Key applications include pathway analysis in B cell malignancies, investigation of CCM2??s role in hematopoietic cell adhesion and migration, and drug discovery targeting the CCM complex or RhoA-ROCK axis. Compatible assays include western blotting for CCM2 and phospho-MLC, RhoA activity measurements, adhesion and transwell migration tests, flow cytometry for integrin expression, co-immunoprecipitation of CCM complex proteins, and RNA-seq transcriptomics. The polyclonal format supports large-scale experiments and reduces clonal variation. For additional information or to order, contact Ascent Research.
