The CNTLN Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblastoid cell line, with targeted disruption of the CNTLN gene. This product provides a heterogeneous pool of edited cells that preserves the genetic diversity inherent to CRISPR/Cas9-mediated gene disruption, making it particularly suitable for robust, population-level studies of centrosome function and genomic integrity without clonal selection artifacts.
The Raji host cell line is an Epstein-Barr virus (EBV)-positive human Burkitt’s lymphoma model with a transformed B lymphoblastoid phenotype. Raji cells express viral latency genes that modulate cell cycle progression and apoptosis pathways, providing a pathophysiologically relevant background for investigating mitotic regulation and oncogenic mechanisms. As a rapidly dividing suspension culture, this line is amenable to assays examining centrosome dynamics, mitotic spindle integrity, and genomic stability.
CNTLN encodes a centrosomal scaffold protein essential for centrosome cohesion and centriole duplication. It forms complexes with CEP250 and NINL that anchor centriolar satellites and facilitate microtubule nucleation, with interactions modulated by upstream kinases including PLK1, CDK2, and Aurora A. CNTLN recruits downstream factors such as CEP250, NINL, PCM1, and gamma-tubulin to the pericentriolar material, coordinating centriole engagement and mitotic spindle assembly. Disruption of CNTLN in this model abrogates these interactions, leading to premature centriole separation, defective spindle formation, and chromosome missegregation, thereby inducing genomic instability.
In the Raji B cell context, CNTLN knockout directly compromises centrosome architecture, resulting in mitotic errors that are especially consequential for lymphoma biology. Burkitt’s lymphoma cells rely on rapid proliferation and are highly sensitive to mitotic disruption; thus, CNTLN loss exacerbates genomic instability, a hallmark of aggressive B cell malignancies. The polyclonal knockout population captures a spectrum of phenotypic severities, mirroring patient tumor heterogeneity and enabling statistically powered studies of centrosome-related pathologies in an EBV-driven oncogenic background.
Researchers can employ these cells in a breadth of applications, including immunofluorescence microscopy for centrosome markers (e.g., gamma-tubulin, pericentrin), flow cytometric cell cycle analysis, and quantification of mitotic index to detect mitotic errors. Western blotting for CEP250 and NINL provides direct biochemical readouts of CNTLN-dependent interactions. Proliferation and colony formation assays in soft agar enable assessment of growth kinetics and tumorigenic potential. This knockout model is a valuable tool for mechanistic dissection of genomic instability in lymphoma, high-throughput screening of small-molecule inhibitors targeting centrosome kinases (PLK1, Aurora A), and exploration of synthetic lethal vulnerabilities in CNTLN-deficient cancers. For detailed protocols, bulk ordering, or technical consultation, please contact Ascent Research.
