CEP164 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblastoid cell line, engineered for research applications requiring loss of CEP164 function. This polyclonal pool offers a mixed genetic background, enabling robust loss-of-function studies without single-cell cloning. The knockout disrupts the CEP164 gene locus, creating a versatile model for investigating centrosome biology, primary cilium assembly, and DNA damage signaling.
The parental Raji cell line is an EBV-positive Burkitt??s lymphoma-derived B lymphocyte model, widely used in immunology, virology, and oncology research. These suspension cells maintain characteristics of mature B cells and exhibit latent Epstein?CBarr virus infection, making them suitable for studies of EBV latency, lymphomagenesis, and B cell signaling. As a lymphoblastoid cell line, Raji cells provide a complementary system to adherent epithelial models for exploring cell-type-specific requirements of centrosomal proteins.
CEP164 encodes a centriolar distal appendage protein essential for primary cilium formation by recruiting TTBK2 to the mother centriole, initiating axonemal extension. It interacts with centriole-associated proteins including CEP83, CEP89, SCLT1, and FBF1 to coordinate ciliogenesis. In the DNA damage response, CEP164 is phosphorylated by ATM and ATR kinases, linking centrosome integrity to genome stability. This activates downstream effectors Chk1, Chk2, and p53, while upstream regulators comprise CDK1/2 and PLK4. Thus, CEP164 integrates cell cycle progression and DNA damage checkpoints.
In Raji B lymphocytes, CEP164 knockout enables dissection of centrosomal functions in a hematopoietic background where ciliary biology is less explored. Although lymphocytes are traditionally considered non-ciliated, recent evidence suggests that primary cilia may transiently appear in certain immune populations; this model facilitates investigation of ciliogenesis and ciliary signaling in B cells. Moreover, because Raji cells are derived from a lymphoma, the knockout provides a relevant system for studying how loss of CEP164-mediated DNA damage signaling contributes to genomic instability in hematologic malignancies. The model also allows assessment of synergistic effects between CEP164 deficiency and EBV-driven oncogenic pathways.
This knockout cell product is suited for a range of experimental applications, including immunofluorescence microscopy to examine centrosome and cilia markers, Western blotting to assess protein-level changes, and RT-qPCR for transcript analysis. Functional assays such as flow cytometry-based cell cycle profiling, apoptosis detection, and DNA damage response evaluation via ??H2AX foci formation are directly applicable. Co-immunoprecipitation can validate CEP164 interactome components, while RNA-seq may reveal transcriptome-wide adaptations. Additionally, these cells can be employed in drug sensitivity screens targeting centrosome integrity or DNA repair pathways, and in investigations of ciliary signaling within the immune system. For further details or technical support, please contact Ascent Research.
