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Cat. No. ARG40702

EFNB1 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

The EFNB1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-engineered polyclonal population of Jurkat T cells with targeted disruption of the EFNB1 gene. EFNB1 encodes ephrin-B1, a transmembrane ligand for EphB receptors that mediates bidirectional signaling controlling adhesion, migration, and activation. These polyclonal knockout cells are ideal for studying the role of EFNB1 in T cell biology, including Eph/ephrin-mediated regulation of Src/FAK and Rho GTPase pathways. Applications include migration and adhesion assays, signaling studies, and inhibitor screening.

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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

    EFNB1

    Gene Identifier

    NCBI Gene ID 1947

    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 EFNB1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat human T lymphocyte cell line. This heterogeneous product contains a mixture of cells with EFNB1 gene disruptions, providing a robust loss-of-function model while avoiding clonal bias. It is suited for functional assays where genetic diversity is advantageous.

The parental Jurkat cell line (clone E6-1) originates from human acute T cell leukemia and is a canonical model for investigating T cell receptor (TCR) signaling, apoptosis, and activation. These suspension cells maintain key signaling pathways, including MAPK/ERK and PI3K/Akt, and are widely used in immunology and oncology research. Their genetic tractability and well-defined background facilitate CRISPR-based gene editing.

EFNB1 (ephrin-B1) is a transmembrane ligand that engages EphB receptor tyrosine kinases to mediate bidirectional signaling, controlling cell adhesion, migration, and axon guidance. In T cells, EFNB1 reverse signaling activates Src family kinases and focal adhesion kinase (FAK), triggering Rho GTPases (RhoA, Rac1) and downstream effectors such as ERK1/2 and Akt. EFNB1 interacts with EphB1?CB4 receptors and PDZ-domain adaptors (GRIP1, syntenin, PDZ-RGS3), and its expression is regulated by TCR/CD28 costimulation, NF-??B, and AP-1. Disruption of EFNB1 abrogates EphB-mediated bidirectional signaling, impairing Src/FAK and Rho GTPase cascades, which leads to altered T cell adhesion, migration, and activation responses.

In the Jurkat T cell context, EFNB1 knockout enables systematic dissection of ephrin-mediated regulation of lymphocyte adhesion, motility, and immune signaling. This model is particularly relevant for studying the role of Eph/ephrin pathways in leukemic cell dissemination and for evaluating their contribution to tumor?Cimmune interactions. Moreover, EFNB1 is associated with cancer metastasis in multiple solid tumors and with developmental disorders such as craniofrontonasal syndrome, highlighting the translational value of this knockout model.

These EFNB1 Knockout Jurkat Polyclonal Cells support a variety of research applications, including analysis of T cell adhesion and migration, mechanistic studies of Eph/ephrin signaling in leukemia, and screening of pathway-specific inhibitors. Compatible assays include Western blotting for EFNB1 and phospho-signaling, RT-qPCR, transwell migration and adhesion assays, flow cytometry for T cell markers and phospho-ERK, co-culture with EphB-Fc, and RNA-seq. For additional information, please contact Ascent Research.

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