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Cat. No. ARG34392

KANK2 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

This product is a CRISPR/Cas9-edited polyclonal Jurkat cell population with targeted disruption of the KANK2 gene. KANK2 is a scaffold protein that regulates actin cytoskeleton dynamics, focal adhesion stability, and cell migration through modulation of the RhoA-ROCK pathway. In the Jurkat T lymphocyte background, KANK2 knockout enables studies of T cell migration, immunological synapse formation, and integrin-mediated adhesion. Key molecular partners include Talin, Actin, and IQGAP1, and typical assays involve RhoA activation and phospho-MLC analysis.

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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

    KANK2

    Gene Identifier

    NCBI Gene ID 25959

    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

KANK2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphocytes with targeted disruption of the KANK2 gene. This knockout model offers a heterogeneous pool of loss-of-function cells, well-suited for population-based functional studies, including signaling and migration analyses.

The Jurkat cell line is a human T cell leukemia-derived model extensively used to study T cell receptor signaling, cytokine production, and apoptosis. As a T lymphocyte model, Jurkat cells recapitulate key aspects of immune cell adhesion, migration, and cytoskeletal dynamics, making them ideal for investigating the molecular regulation of T cell behavior.

KANK2 encodes a scaffold protein that orchestrates cross-talk between integrin adhesion complexes and the actin cytoskeleton. It directly binds to Talin, Actin, Liprin-beta1, IQGAP1, 14-3-3 proteins, and KANK1, thereby linking integrin receptors such as ITGB1 to cortical actin. Functionally, KANK2 promotes RhoA inactivation by recruiting it to actin filaments, attenuating ROCK-mediated phosphorylation of MYPT1 and myosin light chain (MLC) to reduce actomyosin contractility. This activity is modulated by upstream regulators including Src kinase, TGF-beta, and mechanical cues. Key pathway components such as FAK, Vinculin, and ROCK further integrate signals at focal adhesions, influencing cell migration and adhesion dynamics.

In Jurkat cells, loss of KANK2 disrupts the delicate control of actin polymerization and focal adhesion stability, processes vital for T cell migration, immunological synapse formation, and antigen recognition. The knockout model enables dissection of how RhoA-ROCK signaling imbalances alter immune cell adhesion dynamics and mechanosensing, providing insight into T cell activation and cytoskeletal reorganization.

Applications include migration and invasion assays, immunofluorescence staining of focal adhesions, and flow cytometry-based integrin activation profiling. The cells can also be used for RhoA activation assays, phospho-MLC western blotting, and co-immunoprecipitation experiments to probe the KANK2 interactome. Additionally, they provide a platform for drug sensitivity testing against cytoskeletal pathways. For further details, contact Ascent Research.

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