The CPNE8 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population with disrupted CPNE8 gene function, providing a loss-of-function model for functional studies. This heterogeneous cell pool contains diverse editing events, avoiding clonal selection bias and preserving biological variability. The polyclonal format is ideal for pooled screening and bulk biochemical analyses. CRISPR/Cas9-mediated target disruption generates a mixed population of edited Raji cells suitable for investigating copine 8 biology without single-cell cloning artifacts.
Raji cells are an EBV-positive lymphoblastoid line derived from a Burkitt??s lymphoma patient, widely used for B lymphocyte biology research. They grow in suspension, express complement receptors CD21 and CD35, and lack surface immunoglobulin, making them a key model for BCR signaling, apoptosis, antigen presentation, and oncogenesis. Their lymphoma origin and EBV background provide a clinically relevant context for studying tumorigenic mechanisms and viral latency. The CPNE8 knockout pool leverages this well-characterized model to explore lymphoma-associated pathways.
CPNE8 encodes a calcium-dependent phospholipid-binding protein implicated in membrane trafficking, exosome secretion, and integrin-mediated signaling. Upstream, BCR activation and intracellular Ca2+ fluxes engage SRC kinases LYN and SYK. CPNE8 interacts with phosphatidylserine, calcium ions, integrin ?? chains, and TESK1 to coordinate downstream events. It regulates the ESCRT components TSG101 and ALIX, SNAREs SNAP23 and VAMP7, and RAB27A to drive exosome biogenesis and release. Additionally, CPNE8 modulates actin cytoskeleton dynamics and integrin ??1 surface expression, integrating calcium signals with adhesive and secretory functions.
In Raji lymphoma cells, CPNE8 likely couples BCR-driven calcium signaling to exosome secretion and integrin-mediated adhesion, processes critical for lymphoma microenvironment interactions. Knockout of CPNE8 is therefore predicted to impair exosome-mediated communication and reduce integrin-dependent migration and stromal adhesion, potentially affecting tumor progression and drug sensitivity. This polyclonal knockout model enables dissection of copine 8??s role in B-cell lymphoma biology, including exosome-dependent immune evasion and adhesion-linked survival signals.
Key applications include exosome quantification by NTA or ELISA, flow cytometric measurement of surface integrin ??1, and BCR signaling analysis via phospho-SYK and phospho-ERK. The polyclonal cells are well-suited for drug sensitivity screening, transwell migration assays, and Annexin V/PI apoptosis assays. Downstream targets RAB27A and TSG101 can be monitored by RT-qPCR, and actin organization by immunofluorescence. These assays facilitate comprehensive investigation of CPNE8 function in lymphoma. For further technical details, please contact Ascent Research.
