The DTX3L Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes carrying a targeted disruption of the DTX3L gene. This polyclonal knockout cell pool provides a heterogeneous loss-of-function model suitable for studying the role of the interferon-inducible E3 ubiquitin ligase DTX3L in antiviral signaling and B-cell biology. The cells are prepared using CRISPR/Cas9-mediated gene disruption, enabling functional studies without clonal selection biases.
The Raji host cell line is a well-established EBV-positive Burkitt lymphoma model derived from a human B lymphocyte. These suspension lymphoblasts retain key features of B-cell biology, including surface immunoglobulin expression and antigen presentation, making them relevant for studies of B-cell receptor signaling, lymphomagenesis, and immune responses. The EBV-driven background allows investigation of interactions between viral latency and host interferon pathways. As a model of aggressive B-cell lymphoma, Raji cells are widely used in preclinical drug testing and functional genomics.
DTX3L encodes an interferon-inducible E3 ubiquitin ligase that functions as a positive regulator of JAK-STAT signaling downstream of type I interferon receptors. Upon IFN stimulation, DTX3L is transcriptionally upregulated by STAT1 and IRF9, and it forms a complex with PARP9 to mediate ubiquitination of STAT1 and histone H2B. This ubiquitin-dependent mechanism enhances STAT1 phosphorylation and promotes the assembly of ISGF3 complexes, thereby amplifying transcription of interferon-stimulated genes (ISGs). DTX3L also interacts with the E2 ubiquitin-conjugating enzyme UBE2L6, further coupling ubiquitination to antiviral effector programs. These activities position DTX3L as a key amplifier of interferon-driven innate immunity.
In the Raji B-cell lymphoma background, DTX3L disruption helps dissect the intersection of antiviral immunity and oncogenic signaling. EBV-positive Burkitt lymphoma cells often show altered JAK-STAT activity, and DTX3L-mediated STAT1 ubiquitination may influence both antiviral defense and lymphomagenesis. This model enables studies on how DTX3L loss affects ISG profiles, proliferation, and apoptosis. Comparisons between knockout and parental cells can reveal impacts on B-cell receptor signaling, antigen presentation, and cytokine production.
Applications include dissecting type I interferon signaling, validating ubiquitination roles in JAK-STAT activation, and profiling antiviral gene expression. Compatible assays include phospho-STAT1 Western blotting, ISG RT-qPCR, ISRE luciferase reporters, and RNA-seq. Co-immunoprecipitation can probe DTX3L interactions with PARP9, STAT1, and UBE2L6. In B-cell lymphoma research, these cells support proliferation, apoptosis, drug sensitivity screens, and flow cytometric analysis of B-cell markers. For more information, please contact Ascent Research.
