The DNAAF2 Knockout Raji Polyclonal Cells product consists of a genetically heterogeneous population of Raji cells that have undergone CRISPR/Cas9-mediated disruption of the DNAAF2 (dynein axonemal assembly factor 2) gene. This polyclonal knockout format provides a robust loss-of-function model by abolishing DNAAF2 protein expression across a mixed population, enabling researchers to study the functional consequences of DNAAF2 deficiency without clonal isolation artifacts. The cells are supplied as a live polyclonal stock suitable for further expansion and downstream experimentation in cell biology and molecular genetics.
The Raji host cell line is a well-characterized human B lymphocyte line derived from a Burkitt??s lymphoma patient. Raji cells are suspension-adapted, express surface immunoglobulin, and are widely employed in immunology, virology, and oncology research. They provide a consistent and genetically manipulable background for investigating gene function in the context of B cell biology. Although Raji cells are not typically ciliated, their robust growth characteristics and well-documented signaling pathways make them a practical chassis for ectopic expression studies and biochemical analyses of non-ciliary protein functions.
DNAAF2 encodes a cytoplasmic co-chaperone that facilitates the preassembly of axonemal dynein arm complexes, a process critical for motile cilia function. This protein operates within a multimolecular chaperone network, directly interacting with DNAAF1 (LRRC50), DNAAF3, DNAAF6 (Pih1d3), and the heat shock proteins HSP90 and HSP70. DNAAF2 function is transcriptionally regulated by the key ciliogenic transcription factors RFX3 and FOXJ1. Downstream, properly assembled dynein complexes incorporate heavy chains such as DNAH5 and DNAH11 into the axonemal dynein arms. Disruption of DNAAF2 therefore abrogates the formation of functional dynein arms, severely impairing ciliary motility and downstream processes like mucociliary clearance.
In the Raji B lymphocyte background, DNAAF2 knockout serves as a powerful tool for dissecting the chaperone-mediated assembly of dynein complexes independently of ciliogenesis. While Raji cells lack motile cilia, the model permits focused investigation of DNAAF2??s biochemical interactions, co-chaperone activity, and its regulation by upstream transcription factors. This cellular context is particularly advantageous for proteomic analyses, co-immunoprecipitation studies, and high-resolution imaging of protein complexes, providing mechanistic insights that complement studies in ciliated cell types. The model thus aids in understanding the molecular etiology of primary ciliary dyskinesia and Kartagener syndrome at the protein level.
Researchers can utilize DNAAF2 Knockout Raji Polyclonal Cells to explore ciliogenesis mechanisms, model primary ciliary dyskinesia, and screen therapeutic compounds for motile ciliopathies. Representative applications include RT-qPCR and western blotting to confirm DNAAF2 ablation, immunofluorescence staining for acetylated tubulin to assess microtubule stability, ciliary beat frequency analysis in cells engineered to express ciliary proteins, and transmission electron microscopy to visualize axonemal ultrastructure in inducible systems. This versatile model supports the development of novel interventions for dynein arm assembly defects. For detailed product information, protocols, or ordering, please contact Ascent Research.
