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Cat. No. ARG31902

AVL9 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The AVL9 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of the A-549 lung adenocarcinoma cell line, providing a loss-of-function model for the AVL9 gene. AVL9 is a key regulator of cell migration and invasion, acting downstream of EGF, TGF-??, and integrin signals to facilitate vesicle-mediated recycling of integrins and focal adhesion turnover via FAK, Src, and Rho GTPases. This polyclonal knockout model is ideal for studying lung adenocarcinoma metastasis, screening anti-metastatic drugs, and exploring cell motility mechanisms. Applications include wound healing, transwell invasion, and live-cell imaging assays, supported by molecular analyses such as western blotting and immunofluorescence.

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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

    AVL9

    Gene Identifier

    NCBI Gene ID 23080

    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 AVL9 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung adenocarcinoma cell line. This model provides a loss-of-function system for AVL9, generated through CRISPR/Cas9-mediated gene disruption. The polyclonal format offers a heterogeneous knockout pool, minimizing clonal selection bias and enabling robust population-level functional studies.

The A-549 cell line, established from a 58-year-old Caucasian male with lung adenocarcinoma, serves as a widely used epithelial model for human lung cancer. These cells are integral to research in cancer biology, respiratory diseases, and drug development, owing to their well-characterized signaling networks and relevance to adenocarcinoma pathology.

AVL9 is implicated in the regulation of cell migration and invasion through its involvement in vesicle-mediated transport and cytoskeletal dynamics. Acting downstream of EGF, TGF-??, and integrin signaling, AVL9 facilitates the recycling of integrins and membrane components to the leading edge, thereby promoting focal adhesion turnover and actin reorganization. This process engages key effectors including FAK, Src, Rho GTPases (Rac1, Cdc42, RhoA), and matrix metalloproteinases (MMPs), while AVL9 associates with actin, vimentin, and vesicle trafficking proteins. The coordinated activity of downstream pathway components such as ROCK, PAK, talin, and paxillin drives membrane protrusion and sustained cell motility.

In the context of A-549 lung adenocarcinoma cells, disruption of AVL9 compromises the machinery essential for migration and invasion, leading to reduced focal adhesion dynamics and cytoskeletal remodeling. This attenuated motile phenotype makes the knockout cells a valuable platform for investigating the mechanisms underlying metastatic dissemination and for evaluating therapeutic strategies aimed at inhibiting cancer cell motility.

The AVL9 Knockout A-549 Polyclonal Cells are suitable for a range of experimental approaches, including wound healing and transwell invasion assays to assess migratory and invasive capacity, immunofluorescence staining for F-actin to visualize cytoskeletal structures, and phospho-signaling analyses to probe FAK/Src/Rho GTPase pathways. Additional applications encompass western blotting and RT-qPCR for gene expression validation, co-immunoprecipitation for interaction studies, and live-cell imaging to monitor dynamic migration processes. For further details, please contact Ascent Research.

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