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Cat. No. ARG34113

IL15RA Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

CRISPR/Cas9-edited polyclonal knockout A-549 cell population with disruption of IL15RA, encoding the IL-15 receptor alpha subunit. IL15RA transmits IL-15 signals via JAK/STAT, PI3K/AKT, and MAPK pathways, involving effectors such as STAT5 and AKT, and modulates tumor cell survival and cytokine secretion. This model facilitates loss-of-function studies in a widely used lung adenocarcinoma line. Key applications include immune microenvironment research, cytokine signaling analysis, and drug target validation. The polyclonal cells are compatible with Western blotting, RT-qPCR, flow cytometry, proliferation, apoptosis, migration, co-culture, and ELISA assays for probing IL-15/IL-15RA biology.

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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

    Il15ra

    Gene Identifier

    NCBI Gene ID 3601

    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 IL15RA knockout A-549 polyclonal cells are a mixed population of A-549 human lung adenocarcinoma cells with CRISPR/Cas9-mediated disruption of the IL15RA gene. This polyclonal knockout cell population preserves the parental genetic background while introducing a loss-of-function mutation of IL15RA, enabling reliable studies of IL-15/IL-15RA signaling in a relevant epithelial tumor model. The product provides a bulk knockout model free from clonal selection artifacts, suitable for diverse in vitro experimental designs.

A-549 is a human lung adenocarcinoma cell line established from a 58-year-old male, characterized by epithelial morphology, hypotriploid karyotype, and wild-type p53 expression. Widely used as a model of type II alveolar epithelial cells, it is a key tool in respiratory disease and cancer research, including drug metabolism, viral infection, and lung adenocarcinoma biology. This well-characterized background provides a consistent platform for investigating the role of IL15RA in tumor cell behavior.

IL15RA encodes the alpha subunit of the IL-15 receptor, which binds IL-15 and presents it to IL-2RB/IL-2RG, triggering JAK1/JAK3-mediated phosphorylation of STAT5 and STAT3 and activation of PI3K/AKT and RAS/MAPK pathways. The receptor complex engages adaptors TRAF6 and SHC, and downstream targets include BCL-2, MYC, cyclin D1, and SOCS1. IL15RA transcription is regulated by TNF-alpha, interferon-gamma, NF-??B, STAT5, and TGF-beta. In epithelial and immune cells, IL15RA modulates survival, proliferation, and cytokine output, influencing tumor?Cimmune crosstalk.

In A-549 lung adenocarcinoma cells, IL15RA knockout attenuates JAK/STAT, PI3K/AKT, and MAPK signaling downstream of IL-15, impairing cell survival, proliferation, and migration. Altered cytokine secretion, such as reduced IL-10, may reshape the tumor microenvironment and immune interactions. This model is valuable for dissecting the contribution of the IL-15/IL-15RA axis to lung cancer progression, immune evasion, and therapeutic resistance.

Research applications include lung cancer immune microenvironment analysis, cytokine signaling studies, and drug target validation for the IL-15/IL-15RA pathway. The cells support Western blotting for IL15RA and phospho-STAT5, RT-qPCR, flow cytometry, and functional assays for proliferation, apoptosis, migration, and invasion. Co-culture with immune cells and cytokine ELISA profiling further enable investigation of tumor?Cimmune dynamics. For technical inquiries, contact Ascent Research.

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