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Cat. No. ARG33920

ARMC8 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

The ARMC8 Knockout Jurkat Polyclonal Cells are CRISPR/Cas9-edited polyclonal Jurkat T-cell populations with targeted disruption of the ARMC8 gene. This model serves as a loss-of-function tool for investigating the CTLH E3 ubiquitin ligase complex in a human T-cell leukemia background. ARMC8 disruption attenuates Wnt/??-catenin and Akt/mTOR signaling via reduced CTNNB1 stabilization and AKT1 phosphorylation, thereby impairing proliferation and promoting apoptosis in Jurkat cells. This knockout model is employed in cancer research, T-cell signaling studies, and characterization of the CTLH ubiquitin ligase complex.

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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

    ARMC8

    Gene Identifier

    NCBI Gene ID 25852

    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

The ARMC8 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population derived from the Jurkat human T-lymphocyte line, engineered to disrupt the ARMC8 gene. This knockout model provides a heterogeneous pool of cells with targeted gene disruption, enabling robust loss-of-function studies within an immortalized T-cell leukemia background. The polyclonal format preserves genetic diversity while ensuring consistent ablation of ARMC8 function across the population, making it suitable for bulk biochemical and phenotypic analyses.

Jurkat cells are a human CD4+ T-cell leukemia line derived from acute lymphoblastic leukemia, widely used for studying T-cell signaling and apoptosis. They exhibit rapid growth and maintain key oncogenic pathways such as MAPK/ERK and PI3K/Akt, making them a robust model for cancer research. The immortalized nature of Jurkat cells facilitates genetic manipulation and long-term functional studies, providing an ideal host for dissecting genes like ARMC8.

ARMC8 is a constituent of the CTLH E3 ubiquitin ligase complex, where it interacts with MAEA, RMND5A, and WDR26 to stabilize ??-catenin (CTNNB1) and activate Akt/mTOR signaling. Upstream regulators include WNT3A, EGF, and TCF/LEF transcription factors, while miR-940 suppresses ARMC8 expression. Downstream, ARMC8 drives CTNNB1 accumulation and TCF7L2-mediated transcription of CCND1, and promotes phosphorylation of AKT1 and MTOR, thereby enhancing survival and proliferation. Crosstalk with the MAPK/ERK pathway further amplifies oncogenic output. Disruption of ARMC8 uncouples these networks, offering a precise tool for signaling studies.

In the Jurkat T-leukemia context, ARMC8 supports proliferation and apoptosis resistance via ??-catenin and Akt/mTOR. Knockout disrupts these pathways, impairing cell growth and increasing apoptotic susceptibility. This polyclonal model thus enables interrogation of CTLH complex roles in leukemogenesis and identification of ARMC8-dependent vulnerabilities.

This knockout cell population is suitable for Western blotting of CTNNB1 and phospho-AKT1, TOP/FOP luciferase reporter assays, flow cytometry for cell cycle analysis, and Annexin V apoptosis assays. Proliferation and tumorigenicity can be assessed by MTT/CCK-8 and colony formation assays, while co-immunoprecipitation probes CTLH complex assembly. Applications span cancer biology, T-cell leukemia research, and ubiquitin ligase characterization. For further information, contact Ascent Research.

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