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Cat. No. ARG40798

EHD2 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

EHD2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from Jurkat human T lymphocytes, with targeted disruption of the EHD2 gene. EHD2 encodes an ATPase that regulates caveolae stability, endocytic recycling, and actin cytoskeleton remodeling through interactions with caveolin-1, Rac1, and dynamin-2. This loss-of-function model enables investigation of T-cell migration, adhesion, and receptor trafficking, with applications in cancer metastasis, immunology, and drug target validation using assays such as transwell migration, immunofluorescence, and flow cytometry.

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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

    EHD2

    Gene Identifier

    NCBI Gene ID 30846

    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 EHD2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from Jurkat cells, featuring targeted disruption of the EHD2 gene. This product provides a mixed population of edited cells with loss-of-function mutations introduced by CRISPR/Cas9-mediated gene disruption, enabling the study of EHD2-dependent processes without clonal isolation.

The Jurkat host cell line is an immortalized human T lymphoblastoid cell line originally derived from a patient with acute T-cell leukemia. It serves as a well-characterized model for T-cell biology, leukemia research, and immunology, and is extensively used in studies of T-cell signaling, HIV pathogenesis, and lymphocyte activation. The Jurkat background offers a robust platform for investigating the roles of specific genes in T-cell function.

EHD2 is an ATPase that oligomerizes at membrane interfaces to drive tubulation and scission, playing a central role in caveolae stability and endocytic recycling. It is activated downstream of integrin signaling and the small GTPase Rac1, and is regulated by mechanical stress and MRTF transcription factors. EHD2 interacts directly with caveolin-1, dynamin-2, PACSIN2, the Arp2/3 complex, myosin-2, and actin to orchestrate focal adhesion dynamics and cell migration through actin cytoskeleton remodeling. Disruption of EHD2 thus perturbs membrane trafficking and cytoskeletal organization.

In Jurkat T lymphocytes, this knockout model is particularly valuable for dissecting the contributions of caveolae-mediated endocytosis and actin dynamics to T-cell migration, adhesion, and immune signaling. Since lymphocytes depend on precise cytoskeletal rearrangements for surveillance and activation, EHD2 loss enables researchers to explore how endocytic recycling influences T-cell functional responses and the interplay between membrane trafficking and cell motility.

Researchers can apply these polyclonal knockout cells in transwell migration assays to quantify T-cell invasiveness, immunofluorescence to visualize actin and focal adhesion architecture, and flow cytometry to monitor receptor recycling kinetics. The model also supports co-immunoprecipitation to probe EHD2-containing complexes and live-cell imaging to capture membrane dynamics. Typical applications include tumor metastasis research, immune cell trafficking studies, and drug target validation in cancer. For further information, please contact Ascent Research.

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