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Cat. No. ARG31487

ANKRD16 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The ANKRD16 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ANKRD16 scaffold protein. ANKRD16 interacts with DRG2, actin, and tubulin and is regulated by SP1 and AP-1, linking it to cytoskeletal dynamics and signaling. Its disruption in A-549 lung adenocarcinoma cells provides a model for studying protein interaction networks and cancer cell behavior. Ideal for co-immunoprecipitation, western blotting, and functional assays such as proliferation and migration studies, this product supports drug target validation and signaling research in an epithelial lung cancer context. Contact Ascent Research for more information.

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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

    ANKRD16

    Gene Identifier

    NCBI Gene ID 54522

    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 ANKRD16 Knockout A-549 Polyclonal Cells product provides a CRISPR/Cas9-mediated polyclonal ANKRD16 gene-disrupted cell population derived from the human A-549 lung adenocarcinoma cell line. This loss-of-function model enables researchers to investigate the role of ANKRD16 in cellular signaling, protein-protein interactions, and cytoskeletal organization without the constraints of clonal selection. The polyclonal format preserves heterogeneous genetic backgrounds, offering a robust system for studying gene function in a biologically relevant context.

A-549 cells are a well-characterized epithelial cell line originating from a human lung carcinoma, commonly employed as a model for type II alveolar epithelial cells. These cells are widely used in cancer research due to their ability to recapitulate key aspects of lung adenocarcinoma biology, including signal transduction pathways governing proliferation, migration, and survival. The A-549 background is particularly suited for exploring oncogenic mechanisms and evaluating potential therapeutic targets in non-small cell lung cancer.

ANKRD16 encodes a protein containing ankyrin repeat domains that function as a scaffold to mediate assembly of multiprotein complexes. ANKRD16 interacts directly with DRG2, actin, and tubulin, linking it to cytoskeletal dynamics and intracellular trafficking. Its expression is regulated by the SP1 transcription factor and the AP-1 complex in response to cellular stress signals. Functionally, ANKRD16 acts upstream of DRG2-dependent signaling cascades and contributes to actin cytoskeleton reorganization, positioning it as a critical node in coordinating signal transduction with structural changes.

In the A-549 lung cancer cell context, disruption of ANKRD16 is anticipated to impair the formation of protein interaction networks that rely on ankyrin repeat scaffolds, potentially leading to altered DRG2 signaling and compromised actin filament dynamics. This knockout model is thus highly relevant for dissecting how ANKRD16-dependent complexes influence phenotypes such as cell proliferation, adhesion, and migration??processes frequently dysregulated in lung adenocarcinoma. Additionally, because ANKRD16 is also implicated in neuronal development, these cells may serve as a surrogate system for investigating conserved cytoskeletal mechanisms shared between cancer and neurological disorders.

Researchers can utilize these ANKRD16 knockout A-549 polyclonal cells in a wide array of experimental workflows. For protein interaction studies, co-immunoprecipitation and western blotting can validate ANKRD16 binding partners and assess downstream DRG2 signaling. Immunofluorescence microscopy enables visualization of actin and tubulin reorganization. Functional assays, including cell proliferation and migration assays, provide quantitative readouts of phenotypic consequences. This product is also suitable for drug target validation and screening campaigns aimed at modulating ankyrin repeat-mediated pathways. For additional support or custom inquiries, please contact Ascent Research.

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