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Cat. No. ARG33914

ARL2BP Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

ARL2BP Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphoblasts lacking ARL2BP, an effector of ARL2 that regulates mitochondrial fusion (MFN1, MFN2, OPA1) and microtubule dynamics (TBCD, TBCE). ARL2BP mutations are linked to retinitis pigmentosa and Usher syndrome, making this model useful for probing ciliopathy-related mitochondrial pathways in a T-cell context. Derived from a human T-cell leukemia line, this knockout model supports investigation of mitochondrial defects in T-cell signaling, apoptosis, and metabolism. Applications include immunoblotting, immunofluorescence, flow cytometry, and drug response studies.

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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

    ARL2BP

    Gene Identifier

    NCBI Gene ID 23568

    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 ARL2BP Knockout Jurkat Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphoblasts harboring targeted disruption of the human ARL2BP gene. This loss-of-function model enables investigation of ARL2BP functions in a heterogeneous cell pool, eliminating the need for clonal isolation. The polyclonal nature supports population-level assays and minimizes clone-specific artifacts.

The Jurkat cell line is a human T-lymphocyte model derived from a pediatric T-cell leukemia patient. These suspension cells are widely used to study T-cell receptor signaling, apoptosis, and immune activation pathways, offering a robust and transfectable host for gene knockout experiments.

ARL2BP acts as a selective effector of GTP-bound ARL2, localizing to mitochondria and regulating mitochondrial morphology through interactions with fusion proteins MFN1, MFN2, and OPA1. It also associates with tubulin folding cofactors TBCD and TBCE, linking ARL2 signaling to microtubule dynamics. In addition, ARL2BP participates in ciliary transport, and loss-of-function mutations are linked to retinitis pigmentosa and Usher syndrome. Knockout of ARL2BP in this model disrupts the ARL2-ARL2BP-TBCD/TBCE axis, leading to mitochondrial network abnormalities and potential defects in microtubule-dependent processes.

In Jurkat T cells, ARL2BP disruption provides a tool to dissect mitochondrial contributions to T-cell activation and apoptosis. Mitochondrial dynamics are crucial for energy metabolism, calcium homeostasis, and cell death; therefore, ARL2BP knockout may reveal vulnerabilities in leukemia cell survival or drug resistance. This polyclonal model allows correlation of ARL2BP deficiency with altered signaling downstream of the T-cell receptor and other apoptosis regulators, within a well-characterized lymphoid background.

Applications include immunoblotting for ARL2BP and mitochondrial markers, immunofluorescence for mitochondrial morphology, flow cytometry to assess mitochondrial membrane potential and apoptosis, and co-immunoprecipitation of ARL2-ARL2BP complexes. The cells are suitable for functional genomics screens or drug testing focused on mitochondrial pathways in T-cell leukemia. For further information or custom projects, contact Ascent Research.

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