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Cat. No. ARG34166

GOLGB1 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

The GOLGB1 Knockout Jurkat Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population lacking giantin expression in Jurkat T lymphocytes. Giantin is a Golgi membrane protein that interacts with GM130, p115, dynein, and Arf1 to maintain organelle structure and mediate vesicular transport. Knockout disrupts Golgi organization, protein trafficking, and cytokine secretion. This model is valuable for studying Golgi biology, secretory pathways, T cell activation, and cancer. It supports assays such as flow cytometry, western blotting, and T cell activation assays, facilitating research into membrane trafficking dynamics and immune cell function.

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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

    GOLGB1

    Gene Identifier

    NCBI Gene ID 2804

    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 GOLGB1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the GOLGB1 gene in a human T lymphocyte model. This polyclonal pool, derived from Jurkat cells, enables investigation of giantin function while maintaining genetic diversity. The knockout disrupts the gene encoding giantin, a critical Golgi membrane protein, providing a robust tool for examining Golgi organization and membrane trafficking in an immune cell context.

Jurkat cells, a human acute T cell leukemia-derived line, grow in suspension and are a cornerstone for T cell receptor (TCR) signaling and adaptive immunity research. Their well-defined signaling pathways and ease of culture make them an ideal host for studying how genetic disruption of GOLGB1 impacts lymphocyte function. This host background ensures that experimental observations are directly relevant to T cell biology and leukemic transformation.

GOLGB1 encodes giantin, a golgin family protein that maintains Golgi stack integrity and tethers COPI vesicles. It interacts with GM130, p115, dynein, and Arf1, and operates within a network involving Rab GTPases and SNARE proteins. GOLGB1 knockout leads to fragmented Golgi, defective vesicular transport, impaired protein glycosylation, and dysregulated cytokine secretion. Consequently, downstream processes such as surface receptor expression are compromised, underscoring the role of giantin in coordinating membrane trafficking and secretory pathway fidelity.

In Jurkat T cells, GOLGB1 disruption offers a model to dissect how Golgi-dependent trafficking controls immune responses. Proper giantin function is required for surface presentation of TCR components, co-receptors, and adhesion molecules, as well as for secretion of cytokines like IL-2. By ablating giantin, researchers can investigate the impact on T cell activation, signaling, and effector functions, linking Golgi biology to adaptive immunity and leukemia pathology.

The polyclonal knockout cells are applicable to diverse studies: Golgi apparatus organization, vesicle-mediated transport, secretory pathway mechanisms, T cell immunology, and cancer biology. They are suitable for assays including western blotting, RT-qPCR, immunofluorescence, flow cytometry, ELISA, cell viability tests, and T cell activation assays. For drug discovery targeting membrane trafficking, these cells provide a physiologically relevant screening platform. For further information, please contact Ascent Research.

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