The CEP72 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Homo sapiens Raji B lymphocyte cell line, engineered for targeted disruption of the CEP72 gene. This product supplies a heterogeneous pool of cells with loss-of-function modifications at the CEP72 locus, enabling robust functional studies without clonal isolation. The polyclonal format captures a range of editing outcomes, offering a practical model for investigating CEP72-dependent processes in a well-characterized human lymphoma background. The knockout population is suitable for a broad spectrum of assays, including Western blotting, immunofluorescence, and cell cycle analysis, to interrogate centrosome biology and mitotic regulation.
The host Raji cell line is an Epstein-Barr virus-positive Burkitt lymphoma line established from a 12-year-old male patient. These B lymphocytes express surface immunoglobulins and exhibit characteristic features of transformed B cells, making them a widely used model in immunology and cancer research. Raji cells are particularly valuable for studying B-cell signaling, lymphomagenesis, and the mechanisms underlying chromosomal instability in hematological malignancies. Their rapid proliferation and well-documented genetic background facilitate reproducible experimental conditions, including drug sensitivity testing and functional genomics approaches.
CEP72 encodes a centrosomal scaffold protein essential for centriole duplication and microtubule nucleation. It functions by recruiting AURKA and PLK1 to the centrosome through interactions with pericentrin (PCNT) and other core components such as CEP152 and CEP192. Upstream, CEP72 is regulated by cell cycle cues and kinases including CDK1 and PLK1, as well as E2F transcription factors. Downstream, it activates AURKA and mediates PLK1 recruitment, ultimately promoting ??-tubulin complex assembly and mitotic spindle formation. CEP72 thus integrates signals from the cell cycle machinery to coordinate centrosome maturation and bipolar spindle assembly, with disruption leading to mitotic arrest and defects in chromosome segregation.
In the Raji B lymphocyte context, CEP72 knockout is particularly significant for dissecting how centrosome deregulation contributes to lymphoma pathogenesis. Raji cells, like many cancer cells, often harbor supernumerary centrosomes and aberrant mitotic spindles, which drive chromosomal instability and tumor evolution. Loss of CEP72 in this model is expected to exacerbate or alter these phenotypes by disrupting AURKA/PLK1-mediated centrosome maturation, impairing pericentrin-dependent scaffolding. This polyclonal knockout population therefore enables researchers to examine the interplay between CEP72-dependent centrosome functions and B-cell malignancy, including effects on proliferation, apoptosis, and response to microtubule-targeting agents.
This product facilitates a variety of detailed applications, including Western blot analysis of CEP72 and its interacting partners (PCNT, AURKA, PLK1), immunofluorescence microscopy for centrosome markers (??-tubulin, PCNT), and flow cytometry-based cell cycle profiling. Functional assays such as MTT or BrdU proliferation measurements, mitotic index determination, and Annexin V apoptosis detection are readily implemented. The polyclonal knockout cells are also suited for co-immunoprecipitation studies to map CEP72 interaction networks, transcriptome-wide RNA-seq experiments, and drug screening with microtubule inhibitors (e.g., paclitaxel) to assess chemosensitivity. For additional information or customized support, please contact Ascent Research.
