The CENPF Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte line, featuring targeted disruption of the CENPF gene (Centromere Protein F). This polyclonal format provides a heterogeneous pool of cells with CENPF loss-of-function, suitable for studying gene disruption effects without clonal selection bias. The product is supplied as a live-cell suspension and is intended for biomedical research applications focused on mitosis, chromosome biology, and lymphoma pathology.
The Raji cell line originates from a Burkitt lymphoma patient and is characterized by EBV positivity and a suspension lymphoblastoid growth pattern. As B lymphocytes, Raji cells express surface immunoglobulins and exhibit features of antigen presentation, making them a widely used model for B cell biology, lymphoma research, and immunology. Their transformed status and stable karyotype under culture conditions provide a robust platform for examining mitotic processes in the context of hematological malignancy.
CENPF is a large, multifunctional kinetochore-associated protein that plays a pivotal role in chromosome segregation. It functions downstream of cell-cycle regulators such as FOXM1, E2F, CDK1-cyclin B, and RB, and is essential for recruiting the mitotic kinesin CENP-E to kinetochores. Through CENP-E, it facilitates microtubule capture and chromosome alignment, interacting directly with the NDC80 complex component NUF2, as well as with spindle checkpoint proteins BUB1 and Mad2, and the motor protein dynein. The CENPF?CCENP-E?CNDC80 axis is critical for achieving bipolar microtubule attachment and for satisfying the spindle assembly checkpoint, thereby ensuring accurate mitotic progression.
In the Raji lymphoma background, disruption of CENPF is expected to compromise kinetochore-microtubule attachments, leading to mitotic delays, chromosome missegregation, and the potential induction of aneuploidy or apoptosis. Such defects parallel those observed in Str?mme syndrome, a developmental disorder linked to CENPF mutations, and are relevant to the genomic instability characteristic of many cancers, including Burkitt lymphoma. This knockout model therefore provides a tool to dissect the contribution of CENPF-dependent mitotic fidelity to lymphomagenesis and to assess the vulnerability of lymphoma cells to anti-mitotic agents.
This product is suited for a broad range of experimental approaches. Investigators can employ Western blotting and flow cytometry to confirm knockout and assess cell cycle distribution. Immunofluorescence staining enables visualization of mitotic spindle morphology and chromosome alignment defects, while chromosome spread techniques can quantify aneuploidy rates. Viability assays and clonogenic survival studies permit evaluation of drug sensitivity, particularly to spindle poisons, and RNA-seq facilitates transcriptomic profiling of the knockout phenotype. These applications support research into mitotic regulation, cancer cell biology, anti-mitotic drug screening, and lymphoma pathology. For further details or to discuss custom modifications, please contact Ascent Research.
