The CETN2 Knockout Raji Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population generated from Raji B lymphoblastoid cells for targeted disruption of the CETN2 gene in a human Burkitt lymphoma background. This polyclonal knockout cell model comprises a heterogeneous pool of loss-of-function genotypes, enabling robust analysis of CETN2-dependent cellular processes without the selective pressure of clonal expansion.
Raji cells are an Epstein-Barr virus-positive, suspension lymphoblastoid cell line originally derived from a Burkitt lymphoma patient. They exhibit rapid proliferation, constitutive NF-??B signaling, and characteristics of germinal center B cells, making them a widely used model for B-cell malignancies. The EBV-driven transformation recapitulates key features of lymphomagenesis, including dysregulated cell cycle control and altered DNA damage responses, offering a physiologically relevant environment to study centrosome biology in a lymphoma context.
CETN2 encodes centrin-2, a highly conserved calcium-binding protein that localizes to the centrosome and is essential for centriole duplication and proper mitotic spindle formation. Its expression is transcriptionally regulated by E2F transcription factors in a cell cycle-dependent manner, peaking during S and G2 phases. At the centrosome, centrin-2 physically interacts with CP110, CEP152, and CEP63, and is required for the recruitment of PLK4 and SAS-6 to initiate procentriole assembly. In the nucleus, centrin-2 participates in nucleotide excision repair by forming complexes with XPC and RAD23B to recognize UV-induced DNA lesions. Therefore, CETN2 functions as a dual-role protein that couples cell cycle progression with genome integrity maintenance.
In the Raji cell background, characterized by inherent genomic instability due to EBV-driven proliferation, knockout of CETN2 is predicted to exacerbate centrosome duplication defects and mitotic errors, leading to increased chromosomal instability. This polyclonal knockout model permits assessment of CETN2 loss across a spectrum of mutations, providing a more physiologically representative system than single-cell clones for studying centrosome dysfunction in lymphomagenesis. Furthermore, the proficiency of Raji cells in DNA damage signaling makes this model suitable for investigating centrin-2’s contribution to DNA repair pathways and exploring potential synthetic lethal interactions relevant to targeted lymphoma therapy.
Research applications include centrosome biology, cell cycle regulation, and DNA repair mechanism studies. Researchers can utilize western blotting for CETN2, immunofluorescence staining for centriole markers such as CETN2 and CP110, cell cycle analysis by flow cytometry, DNA damage assessment using ??-H2AX, and apoptosis assays. The model also facilitates drug screening for centrosome-targeting agents and qPCR-based analysis of CETN2 transcription. These polyclonal knockout cells empower mechanistic dissection of centrin-2 function and provide a platform for therapeutic target validation in lymphoma. For additional information, please contact Ascent Research.
