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Cat. No. ARG33716

ACBD3 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

CRISPR/Cas9-edited polyclonal knockout of the ACBD3 gene in Jurkat human T cells, a model for Golgi biology and T-cell signaling. ACBD3 encodes a Golgi-associated protein that binds acyl-CoA and interacts with giantin (GOLGB1) and HSP90 to maintain Golgi structure and regulate lipid metabolism and steroidogenesis. Loss of ACBD3 leads to Golgi fragmentation and impaired secretion. These polyclonal knockout cells enable investigation of Golgi-dependent trafficking, cytokine secretion, and viral replication in an immune cell context. Applications include Western blot, immunofluorescence, flow cytometry, and viral assays, making them suitable for research in immunology, virology, and cancer biology.

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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

    ACBD3

    Gene Identifier

    NCBI Gene ID 64746

    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 ACBD3 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population for loss-of-function studies of the ACBD3 gene in a human T-cell line. This heterogeneous pool of Jurkat cells carries targeted gene disruption, enabling investigation of ACBD3 deficiency without clonal selection. The polyclonal format maintains population diversity, suitable for experiments not requiring clonal uniformity while reliably probing ACBD3-dependent pathways.

The parental Jurkat cell line is an immortalized T-lymphocyte line from a T-cell leukemia patient, widely used to study T-cell receptor signaling, apoptosis, and HIV infection. Its robust growth and well-mapped signaling networks make it ideal for examining immune cell functions and secretory pathways. Employing Jurkat for ACBD3 knockout permits exploration of Golgi biology in the context of T-cell physiology.

ACBD3 (GCP60) is a Golgi-associated acyl-CoA binding protein that interacts with giantin (GOLGB1) to maintain Golgi stacking and functions as a co-chaperone for HSP90AA1. It promotes maturation of clients like CYP11A1 and LDL receptor, and is transcriptionally regulated by SREBP2 in response to cholesterol. Downstream, ACBD3 governs Golgi morphology, secretory transport, and lipid metabolism. It also binds viral proteins (enterovirus 3A, HCV NS5A), implicating it in replication. Knockout of ACBD3 causes Golgi fragmentation, impaired secretion, and lipid dysregulation, highlighting its scaffolding role at the Golgi?CHSP90 interface.

In Jurkat T cells, ACBD3 knockout disrupts Golgi integrity, potentially impairing cytokine secretion, surface receptor presentation, and apoptotic signaling. This model is valuable for dissecting Golgi-dependent steps in T-cell activation and for studying host factors in enterovirus/HCV replication, as these viruses exploit ACBD3. Additionally, it can inform on ACBD3??s role in leukemogenesis and neurodevelopment due to its involvement in HSP90 chaperone cycles and steroidogenesis.

Applications include Western blotting and immunofluorescence for ACBD3 and giantin to confirm knockout and visualize Golgi fragmentation. Flow cytometry can assess surface LDL receptor levels and Annexin V apoptosis, while co-immunoprecipitation probes HSP90 interactions. Cytokine ELISAs and RT-qPCR measure functional secretion and transcriptional changes. Viral replication assays extend utility to virology. These polyclonal knockout cells provide a versatile tool for cell biology, immunology, and drug discovery. For further details, contact Ascent Research.

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