The NUDCD2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited human B lymphocyte population with targeted gene disruption of NUDCD2. This polyclonal knockout pool provides a loss-of-function system for studying NUDCD2 roles in dynein complex biology and B-cell lymphoma pathogenesis.
Derived from a Burkitt lymphoma patient, the Raji cell line is an EBV-positive, suspension-growing B-lymphoblastoid model expressing surface IgM and hallmark B-cell markers. It is widely used in immunology and cancer research as a mature B-cell model for investigating lymphomagenesis and EBV-related mechanisms. The Raji line proliferates in suspension and retains many features of germinal center B cells, making it a robust platform for examining B-cell-specific gene functions in a cancer-relevant setting.
NUDCD2 functions as a co-chaperone that stabilizes cytoplasmic dynein intermediate chains, facilitating assembly of functional dynein motor complexes required for microtubule-based transport, mitotic spindle integrity, and primary cilia formation. It directly binds to dynein intermediate chain DYNC1I2 and heavy chain DYNC1H1, and collaborates with NUDC, LIS1 (PAFAH1B1), and NDE1 at centrosomes. Transcriptional control by FOXJ1 and RFX factors governs its expression in ciliated cells, while CDK1-mediated phosphorylation modulates its mitotic role. As a component of the intraflagellar transport machinery, NUDCD2 influences the Hedgehog signaling pathway through interactions with SMO, GLI transcription factors, IFT80, IFT88, and dynein-2 subunit DYNC2H1.
In the Raji B-lymphoblastoid background, NUDCD2 disruption allows dissection of its mitotic and trafficking functions within a lymphoma model. Given that NUDCD2 overexpression has been linked to B-cell malignancies, these polyclonal knockout cells are valuable for assessing effects on proliferation, genomic stability, and drug sensitivity. Although Raji cells do not normally form primary cilia, inducible ciliogenesis systems can be employed to study NUDCD2-dependent ciliary trafficking and signaling in this cellular context.
Applications include co-immunoprecipitation and immunofluorescence assays to probe dynein complex assembly, flow cytometry for cell cycle and apoptosis analysis, and RNA-seq for global transcriptomic profiling. The model supports screening for dynein-targeted inhibitors and evaluation of NUDCD2 in B-cell lymphoma pathogenesis. Standard readouts such as Western blotting, RT-qPCR, and cell viability assays complement these studies. For further information, please contact Ascent Research.
