The CNTRL Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for studying centrosome biology and cytokinesis. This product targets the CNTRL gene in the Raji cell line, generating a heterogeneous pool of cells with disrupted CNTRL expression. This polyclonal knockout approach provides a robust model for investigating the functional consequences of CNTRL loss in a B lymphocyte context without the biases of single-cell cloning. The knockout cell pool is suitable for a range of biochemical, cell biological, and genomic assays to elucidate the role of centriolin in cell division and centrosome dynamics.
The Raji host cell line is a human B lymphocyte derived from a Burkitt lymphoma, an aggressive B-cell malignancy. Raji cells are EBV-positive and retain features of mature B cells, including the capacity for antibody production and humoral immune functions. As a suspension cell line, Raji is widely used in immunology and cancer research, particularly for studying B-cell receptor signaling, apoptosis, and lymphomagenesis. Their well-characterized karyotype and rapid proliferation make them an ideal model for investigating cell cycle regulation and centrosome-driven processes relevant to hematopoietic cancers.
CNTRL encodes centriolin, a centrosomal scaffold that recruits CEP110 and Ninein to the mother centriole, ensuring centrosome cohesion and proper abscission during cytokinesis. Its expression is driven by E2F and FOXM1 transcription factors, and its activity is regulated via phosphorylation by PLK1 and Aurora A kinases. Centriolin interacts with CEP250 and functions downstream of PLK4 in centriole duplication, linking these pathways to cytokinesis and ciliogenesis.
In the Raji B lymphocyte background, disruption of CNTRL is expected to impair centrosome duplication and cytokinesis, leading to mitotic defects such as multipolar spindles, chromosome missegregation, and failed abscission. These cellular abnormalities are directly relevant to cancer biology, as centrosomal aberrations are a hallmark of many malignancies, including Burkitt lymphoma. Additionally, since CNTRL is implicated in ciliogenesis, this knockout model may reveal connections between centrosomal dysfunction and ciliopathy-related mechanisms in hematopoietic cells, a cell type not traditionally associated with primary cilia but where centrosomal proteins may influence cell polarity and migration.
Researchers can employ these polyclonal knockout cells for centrosome isolation and proteomics, immunofluorescence localization, flow cytometry cell cycle analysis, and cytokinesis assays. They are also suited for RNA-seq and western blotting to map pathway alterations. Applications include centrosome biology, B-cell lymphoma pathogenesis, and drug target discovery, especially regarding PLK1 and Aurora A inhibitors. For further information, contact Ascent Research.
