The DTWD1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblastoid cell line, engineered to disrupt the DTWD1 gene. This product provides a heterogeneous pool of cells with targeted gene disruption, enabling the study of DTWD1 loss-of-function in a lymphoma-relevant context. The polyclonal nature allows researchers to capture a range of knockout efficiencies and phenotypes, making it a versatile tool for functional genomics and cancer biology investigations.
Raji is an Epstein-Barr virus (EBV)-positive B lymphoblastoid cell line originally established from a Burkitt lymphoma patient. It displays characteristic B-cell markers and grows in suspension, offering a robust and well-characterized model for B-cell malignancies. The cell line is widely employed in immunological and oncological research, particularly for studying lymphomagenesis, signal transduction, and gene function. Its EBV-positive status also provides a relevant background for investigating viral interactions in B-cell transformation.
DTWD1 encodes a probable S-adenosylmethionine-dependent methyltransferase that catalyzes wybutosine formation at position 37 of tRNA-Phe, a modification critical for translational fidelity and efficiency. It functions within the wybutosine biosynthesis pathway alongside TYW1, TYW3, and TYW4, utilizing S-adenosylmethionine as a methyl donor. Its downstream consequences include modulation of tRNA-Phe function and translation of mRNAs enriched for specific codons, indirectly influencing cell cycle regulators. Although upstream regulatory factors and interacting proteins of DTWD1 remain poorly defined, the enzyme is linked to cell proliferation control, with knockout studies suggesting a tumor-suppressive role.
In the context of B-cell lymphomas such as Burkitt lymphoma, dysregulated translation is increasingly recognized as a driver of oncogenesis. The DTWD1 knockout model in Raji cells is particularly significant because it permits the dissection of how tRNA modifications impact translational control in a B-cell malignancy background. By eliminating DTWD1 function, researchers can investigate how loss of wybutosine modification alters the expression of proliferation-associated proteins and contributes to lymphoma biology. This model may also reveal dependencies on translational fidelity mechanisms specific to EBV-positive lymphoblastoid cells.
This polyclonal knockout cell population is ideally suited for functional characterization of DTWD1 in Burkitt lymphoma, target validation for tRNA-modifying enzymes, and mechanistic studies of translation control in cancer. Representative experimental approaches include RT-qPCR and western blot for expression analysis, MTT and flow cytometry for proliferation and cell cycle assessment, HPLC-mass spectrometry for tRNA modification analysis, luciferase reporter assays for translation efficiency, and xenograft models for in vivo tumor growth studies. For further inquiries, please contact Ascent Research.
