The CCDC91 Knockout Raji Polyclonal Cells product comprises a heterogeneous pool of Raji B lymphocytes engineered via CRISPR/Cas9-mediated disruption of the CCDC91 gene. This polyclonal knockout population provides a consistent loss-of-function model for investigating CCDC91 functions in centrosome biology and cell cycle regulation, without the need for single-cell cloning.
The parental Raji cell line is a human B-lymphoblastoid model derived from a Burkitt lymphoma patient. EBV-positive and suspension-adapted, these cells are extensively used in immunology and cancer research to study B-cell malignancies, immune signaling, and viral oncogenesis.
CCDC91 is a centrosomal coiled-coil protein that interacts with PCM1, CEP135, CEP152, CEP290, and Pericentrin to maintain centrosome integrity. Phosphorylation by CDK1 and PLK1 and transcriptional control by E2F1 and FOXM1 regulate its activity. CCDC91 is essential for proper mitotic spindle assembly and chromosome segregation; it governs the spindle assembly checkpoint through modulation of BUB1, MAD2L1, and Cyclin B1. Knockout triggers caspase-3-dependent apoptosis, underscoring its role in mitotic fidelity and survival.
In Raji B-cells, CCDC91 disruption models centrosome fragmentation and mitotic arrest characteristic of mitotic catastrophe. Given the prevalence of centrosomal abnormalities in B-cell lymphomas, this knockout system allows interrogation of mechanisms linking centrosome dysfunction to aneuploidy and tumorigenesis. The EBV-positive background further enables investigation of viral?Chost interactions affecting centrosome biology.
Applications include immunoblotting for mitotic markers, RT-qPCR for CCDC91 transcript levels, immunofluorescence microscopy of centrosome and spindle architecture, flow cytometric analysis of cell cycle distribution, Annexin V apoptosis assays, and MTS proliferation measurements. These cells also facilitate drug response profiling against anti-mitotic chemotherapeutics. For additional information, please contact Ascent Research.
