The CFAP100 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the human CFAP100 gene in Raji B lymphocytes. This polyclonal format provides a heterogeneous pool of cells, each carrying distinct CRISPR/Cas9-mediated modifications at the CFAP100 locus, enabling loss-of-function studies without a clonal selection bias. The product serves as a reliable model for dissecting the biological functions of CFAP100, a cilia- and flagella-associated protein, in a non-ciliated cell context and supports bulk-scale genomic and pharmacological investigations.
Derived from an EBV-positive Burkitt’s lymphoma patient of African origin, the Raji cell line is a suspension-adapted B-lymphocyte model with mature B-cell characteristics. These cells are extensively characterized and widely utilized for studying B-cell malignancies, signal transduction, and host?Cvirus interactions. Their rapid proliferation, ease of culture in suspension, and well-annotated molecular profile make them an ideal host for CRISPR/Cas9-mediated gene disruption, facilitating reproducible assays in immunology and cancer biology.
CFAP100 encodes an axonemal protein essential for the assembly and motility of motile cilia and sperm flagella. In ciliated cells, its expression is transcriptionally activated by FOXJ1 and RFX3, and the protein interacts with structural components such as CCDC39, CCDC40, and the dynein heavy chain DNAH5 to organize dynein arms and regulate ciliary beat frequency. CFAP100 functions downstream of Notch signaling and participates in intraflagellar transport complexes containing IFT88. Although its canonical roles are cilia-dependent, emerging data suggest that in non-ciliated cells, CFAP100 may influence cell cycle progression and MAPK/ERK pathway activity, though the direct molecular mechanisms remain to be fully elucidated.
Because Raji cells lack primary cilia, this knockout model uniquely allows investigation of non-ciliary CFAP100 functions within a lymphoma-relevant background. Disruption of CFAP100 could perturb cell cycle checkpoints, alter MAPK/ERK signaling, or affect apoptotic responses, potentially revealing previously unrecognized roles in lymphomagenesis or tumor progression. This system thus provides a valuable bridge between classical ciliary biology and hematological malignancy research, enabling the study of a ciliary protein??s impact in a setting where its canonical organelle is absent.
Researchers can apply this polyclonal knockout population to a wide range of experimental workflows, including RNA-seq-based transcriptomic profiling, Western blotting, RT-qPCR, and high-content phenotypic assays such as flow cytometric analysis of viability, apoptosis, and cell cycle distribution. The polyclonal nature also supports pooled functional genomics screens and drug sensitivity testing to identify synthetic lethalities or novel therapeutic targets in B-cell lymphoma. Additional uses encompass exploring interactions between EBV latency programs and CFAP100 loss, or evaluating potential ciliopathy-related processes in a non-ciliated model. For further information, please contact Ascent Research.
