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Cat. No. ARG34361

ISOC1 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

ISOC1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte line. ISOC1 encodes a mitochondrial deamidase that deamidates the viral RNA sensor RIG-I, suppressing MAVS-dependent activation of IRF3 and NF-??B and reducing type I interferon (IFN-??) induction. This model facilitates study of innate immune regulation in a T cell context. Applications include dissection of the RIG-I/MAVS/IRF3 signaling axis, screening of immunomodulatory compounds, and viral infection assays, supported by techniques such as Western blotting, RT-qPCR, and flow cytometry. Contact Ascent Research for further details.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Jurkat

    Cell Type

    T cell line

    Sex of Donor

    Male

    Age

    14 years

    Derived From Site

    In situ; Peripheral blood

    Gene Name

    ISOC1

    Gene Identifier

    NCBI Gene ID 51015

    Growth Mode

    Suspension

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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

ISOC1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat T lymphocyte line, featuring disruption of the ISOC1 gene. This heterogeneous loss-of-function model, produced via CRISPR/Cas9-mediated gene disruption, avoids clonal artifacts and enables robust study of ISOC1-dependent mechanisms. Supplied as ready-to-use cells, they facilitate investigations into innate immune signaling and RIG-I-mediated responses.

The parental Jurkat line is an immortalized CD4+ T cell leukemia line from a 14-year-old male patient, widely used for T cell signaling and leukemia research. Jurkat cells exhibit features of activated T lymphocytes, including cytokine production and intact signaling pathways, providing a well-characterized platform for studying mitochondrial antiviral immunity in a T cell context.

ISOC1 encodes a mitochondrial deamidase that negatively regulates antiviral innate immunity by deamidating the viral RNA sensor RIG-I. This modification attenuates RIG-I activation and downstream signaling via MAVS, reducing the activation of TBK1 and IKK??, which in turn limits the phosphorylation and nuclear translocation of IRF3 and NF-??B, and suppresses type I interferon (IFN-??) induction. ISOC1 thus functions upstream of the RIG-I/MAVS/IRF3 axis to dampen antiviral responses. The gene is itself induced by type I interferons, creating a feedback loop, and its activity is modulated by viral RNA, positioning it as a key mitochondrial checkpoint.

In Jurkat T cells, ISOC1 knockout provides a model to dissect mitochondrial deamidase regulation of RIG-I signaling in a T lymphocyte background. This enables study of innate immune modulation in cells that bridge adaptive and innate immunity, and is particularly relevant for exploring immune dysregulation and viral evasion mechanisms, given Jurkat cells’ competent mitochondrial and interferon-responsive machinery.

Key applications include dissection of the RIG-I/MAVS/IRF3 pathway, screening of ISOC1-targeted modulators, and viral infection assays to assess antiviral responses. Representative techniques such as Western blotting for pathway proteins, RT-qPCR for IFN-?? and ISGs, luciferase reporter assays, co-immunoprecipitation of ISOC1 and RIG-I, and flow cytometry for phospho-IRF3 enable detailed mechanistic studies. These assays support rigorous antiviral signaling research in a tractable T cell system. For further information, please contact Ascent Research.

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