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Cat. No. ARG33570

GOLGA3 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The GOLGA3 Knockout A-549 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout model of the Golgi structural protein golgin-160 in A-549 non-small cell lung cancer cells. GOLGA3 maintains Golgi ribbon integrity and is cleaved by caspase-3 and caspase-7 during apoptosis, linking organelle fragmentation to cell death signaling. Interactions with GOLGA2 and GORASP1 are disrupted upon cleavage, affecting vesicular trafficking and apoptosis amplification. This model is suited for investigating Golgi organization, secretion, and apoptosis resistance in cancer, using assays such as immunofluorescence, western blot, and viability tests.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    A549

    Sex of Donor

    Male

    Age

    58 years

    Derived From Site

    Lung

    Gene Name

    GOLGA3

    Gene Identifier

    NCBI Gene ID 2802

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM

    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 GOLGA3 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung adenocarcinoma cell line, serving as a loss-of-function model for the Golgi structural protein golgin-160 (GOLGA3). This polyclonal knockout population facilitates the study of GOLGA3 in Golgi ribbon maintenance, vesicular trafficking, and apoptosis signaling without clonal bias.

A-549 cells, isolated from a 58-year-old male lung adenocarcinoma, are a widely used model for non-small cell lung cancer (NSCLC) with alveolar basal epithelial characteristics. They are employed extensively to investigate oncogenic signaling, drug response, and apoptotic pathways, providing a relevant background for examining GOLGA3??s role in cancer cell biology.

GOLGA3 (golgin-160) is a Golgi resident protein critical for maintaining Golgi ribbon structure and mediating vesicle transport. Upon apoptotic stimuli, it is cleaved by caspase-3 and caspase-7, leading to Golgi fragmentation and amplification of apoptosis signaling. It interacts with GOLGA2 (GM130) and GORASP1 (GRASP65), and its cleavage disrupts these complexes. GOLGA3 functions downstream of caspase activation and upstream of Golgi disassembly, altered secretion, and impaired apoptosis. Pathway components include GOLGA2, GORASP1, CASP3, Rab GTPases, and COPI/COPII coats, highlighting its role in Golgi organization and transport.

In A-549 cells, GOLGA3 knockout enables investigation of the interplay between Golgi integrity and cancer cell survival. GOLGA3 is implicated in apoptosis resistance through caspase-mediated cleavage, linking organelle disassembly to apoptotic amplification. In NSCLC, dysregulated apoptosis is a hallmark of progression and therapy resistance. Additionally, autoantibodies to golgins like GOLGA3 are found in autoimmunity, extending this model??s relevance to golgin autoimmunity research. Disrupting GOLGA3 allows assessment of Golgi fragmentation effects on secretion and drug sensitivity.

Researchers can use these cells for immunofluorescence microscopy with markers like GM130, western blotting for GOLGA3 and cleaved fragments, apoptosis assays (Annexin V, caspase-3 activation), cell viability assays, and secretion assays (e.g., luciferase secretion). The polyclonal nature supports population-level studies, suitable for high-content screening or pooled functional genomics. For technical inquiries, please contact Ascent Research.

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