The DTX3L Knockout Jurkat Polyclonal Cells are a polyclonal population of Jurkat T lymphocytes engineered with CRISPR/Cas9 to disrupt the endogenous DTX3L gene. This polyclonal knockout product provides a heterogeneous cell pool in which the targeted locus has been edited, enabling functional analyses without the genetic uniformity of a clonal line. It serves as a loss-of-function model for investigating the roles of DTX3L in immune signaling and genome maintenance.
Jurkat is an immortalized human T lymphocyte cell line derived from the peripheral blood of a patient with acute T-cell leukemia. As a well-characterized model of T-cell receptor signaling, apoptosis, and leukemogenesis, Jurkat cells express key downstream effectors of the interferon and DNA damage response pathways, making them a suitable host for DTX3L knockout studies.
DTX3L encodes an interferon-inducible E3 ubiquitin ligase that assembles a multiprotein complex with the ADP-ribosyltransferase PARP9 (BAL1) and the E2 conjugating enzyme UBE2L6. Upon stimulation by type I interferon (IFN???/??) through the IFNAR1?CJAK1?CTYK2 axis or by IFN??? via STAT1 homodimers, DTX3L is transcriptionally upregulated. The DTX3L?CPARP9 complex then catalyzes two key ubiquitination events: monoubiquitination of histone H2B at DNA double-strand breaks, which promotes the recruitment of DNA repair proteins such as 53BP1 and the formation of ???H2AX foci, and polyubiquitination of STAT1, earmarking it for proteasomal degradation and thus dampening interferon signal transduction. Additional interactions with the ubiquitin-like protein ISG15 and the DNA damage kinase ATM place DTX3L at the intersection of innate immunity and genomic stability.
In the Jurkat T?cell leukemia background, disruption of DTX3L allows dissection of how this E3 ligase contributes to the regulation of interferon responsiveness, DNA repair fidelity, and cell survival. Because DTX3L has been implicated in lymphomagenesis and autoimmune pathology, the knockout model provides a platform for studying oncogenic signaling networks, resistance to genotoxic chemotherapy, and the balance between immune activation and negative feedback in a malignant T?cell context.
Representative applications include western blotting and flow cytometry to assess STAT1 phosphorylation and DTX3L/PARP9 expression, RT?qPCR of interferon?stimulated genes, co?immunoprecipitation of the DTX3L?CPARP9 complex, immunofluorescence detection of ???H2AX foci following ionizing radiation or drug treatment, in vitro ubiquitination assays, and cell proliferation or apoptosis analyses. This polyclonal knockout cell pool thus supports mechanistic studies of ubiquitin?mediated signaling, DNA repair, and interferon regulation. For further information, please contact Ascent Research.
