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Cat. No. ARG39957

DTX3L Knockout HEK293T Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Kidney

The DTX3L Knockout HEK293T Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal population with disrupted expression of the DTX3L E3 ubiquitin ligase. This loss-of-function model in HEK293T cells, a high-transfection human embryonic kidney line, enables detailed study of DTX3L in interferon signaling, ubiquitination, and DNA damage repair. DTX3L partners with PARP9 and is induced by STAT1/IRF1 downstream of IFN-??. Applications include functional dissection of the DTX3L?CPARP9 complex, profiling of ubiquitination substrates, and antiviral response screening. These knockout cells are valuable for drug target validation in cancer and infectious diseases, supporting assays such as co-immunoprecipitation, Western blotting, and RT-qPCR.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HEK293T

    Sex of Donor

    Female

    Age

    Fetus

    Derived From Site

    Fetal kidney

    Gene Name

    DTX3L

    Gene Identifier

    NCBI Gene ID 151636

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

DTX3L Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population with disrupted DTX3L gene expression, enabling loss-of-function investigation of this E3 ubiquitin ligase in a widely used human embryonic kidney cell model. The polyclonal format provides a heterogeneous collection of edited cells, avoiding clonal bias while ensuring robust knockout effects across the population.

HEK293T cells originated from human embryonic kidney epithelium transformed with adenovirus 5 DNA and constitutively express the SV40 large T antigen. This enables episomal plasmid replication and yields exceptionally high transfection efficiency and recombinant protein production, making HEK293T a premier host for viral packaging, biochemical reconstitution, and cell-based assays.

DTX3L encodes a RING-type E3 ligase that partners with PARP9 to mediate ubiquitination of target proteins, prominently histone H4. The DTX3L-PARP9 complex is transcriptionally induced by interferon-?? (IFN-??) through the JAK-STAT pathway: IFN-?? receptor engagement activates JAK1/2 kinases, leading to STAT1 phosphorylation, nuclear translocation, and cooperative binding with IRF1 at the DTX3L promoter. NF-??B further augments DTX3L expression. Functionally, DTX3L regulates ISG15 conjugation, antiviral gene programs, and DNA damage repair, placing it at the nexus of innate immunity and genome stability.

In the HEK293T background, which maintains intact interferon and NF-??B signaling circuits, DTX3L knockout provides a clean genetic platform to dissect ubiquitin-dependent immune regulation. The model permits detailed mapping of DTX3L?CPARP9 interaction networks, substrate identification by ubiquitin proteomics, and interrogation of signaling crosstalk between DNA damage and antiviral responses without interference from endogenous DTX3L.

Applications include Western blot analysis of downstream ubiquitination events, co-immunoprecipitation to probe PARP9 complex assembly, RT-qPCR profiling of interferon-stimulated genes, and immunofluorescence tracking of chromatin-associated DTX3L. These cells are also ideal for antiviral compound screening, DNA damage response quantification, and validation of DTX3L as a therapeutic target in cancer or viral pathogenesis. For additional technical information, please contact Ascent Research.

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