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Cat. No. ARG39859

DST Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

The DST Knockout Jurkat Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphocytes with disrupted dystonin expression, a key cytoskeletal linker protein. Dystonin connects intermediate filaments to actin and microtubules through interactions with plectin, BPAG2, and integrin ??6??4, and its loss compromises cell adhesion and mechanical stability. Researchers can use this model for Western blotting, immunofluorescence, adhesion and migration assays, apoptosis profiling, and rescue screening. For inquiries, contact Ascent Research.

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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

    DST

    Gene Identifier

    NCBI Gene ID 667

    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 DST Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the DST gene in Jurkat T lymphocytes. DST encodes dystonin, a plakin family cytoskeletal linker that connects intermediate filaments to actin and microtubules. This product comprises a heterogeneous pool of Jurkat cells with CRISPR/Cas9-mediated disruption of the DST locus via transient Cas9/sgRNA delivery, avoiding clonal selection to preserve a diverse loss-of-function allele spectrum.

Jurkat cells are an immortalized human T lymphocyte line derived from peripheral blood of a 14-year-old male with acute T-cell leukemia. Aneuploid and expressing constitutively active IL-2 receptor, Jurkat cells are a widely used model for T-cell receptor signaling, apoptosis, and HIV infection studies. Their robust growth and well-characterized signaling cascades make them an ideal host for examining cytoskeletal dynamics in immune cells.

Dystonin is a critical cytoskeletal integrator that physically tethers keratin intermediate filaments to actin and microtubule networks. It interacts with plectin, BPAG2/COL17A1, and integrin ??6??4, anchoring the keratin cytoskeleton to adhesion complexes. Regulated by TP53 and cellular stress, dystonin loss compromises cytoskeletal stability, disrupts cell adhesion, and impairs resilience to mechanical force. The dystonin-BPAG2-integrin ??6??4-keratin axis represents a key structural pathway, with dystonin acting upstream of adhesion complex assembly and downstream of stress signals to maintain cellular integrity.

In Jurkat T cells, dystonin??s contribution to adhesion and cytoskeletal organization remains poorly defined, yet its disruption is expected to influence T-cell adhesion, migration, and mechanotransduction. Because dystonin links to TP53-mediated apoptosis, this knockout model allows dissection of how cytoskeletal defects intersect with death signaling in a leukemic T-cell context. The polyclonal nature provides a realistic spectrum of loss-of-function effects, enhancing the study of heterogeneous responses.

This product supports diverse assays, including Western blotting for dystonin confirmation, immunofluorescence for cytoskeletal integrity, cell adhesion and migration/invasion assays, and flow cytometry for apoptosis markers. RT-qPCR can monitor downstream gene expression, while the model is suitable for genetic or chemical rescue screening. For further technical details, contact Ascent Research.

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