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Cat. No. ARG36564

IL1R1 Knockout NCI-H1703 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Squamous cell carcinoma

The IL1R1 Knockout NCI-H1703 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population with disruption of the IL1R1 gene in a human lung squamous cell carcinoma model. IL1R1 encodes the type I IL-1 receptor that transmits pro-inflammatory signals via MYD88, IRAKs, and TRAF6 to activate NF-??B and MAPK cascades, driving IL-6 and TNF-?? production. This knockout model is ideal for studying IL-1-mediated pathways in cancer inflammation, validating drug targets, and performing signal transduction research. Key applications include western blotting, ELISA, NF-??B reporter assays, and functional studies such as proliferation and migration assays. For more information, contact Ascent Research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    NCI-H1703

    Sex of Donor

    Male

    Age

    54 years

    Derived From Site

    In situ; Lung

    Gene Name

    IL1R1

    Gene Identifier

    NCBI Gene ID 3554

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    Supplement(s)

    10% Fetal Bovine Serum, 1% Glutamine, 1% Sodium Pyruvate, 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 IL1R1 Knockout NCI-H1703 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of IL1R1 in the NCI-H1703 human non-small cell lung carcinoma line. This loss-of-function model abrogates functional type I interleukin-1 receptor (IL-1R1) expression, enabling investigation of IL-1 signaling dependency without pharmacologic inhibition. As a heterogeneous pool of knockout cells, it captures population-level editing outcomes and reduces clonal artifacts, offering advantages for studying collective cellular responses.

NCI-H1703 is a widely used squamous cell lung carcinoma line that retains key malignant epithelial features, including robust in vitro growth and invasive potential. It serves as a relevant model for lung cancer biology, particularly for studying tumor cell-intrinsic signaling, the inflammatory microenvironment, and therapeutic responses. Its genetic and phenotypic characteristics make it well-suited for CRISPR-based gene editing to dissect pathway contributions to cancer phenotypes.

IL1R1 encodes the primary receptor for interleukin-1 (IL-1?? and IL-1??), initiating pro-inflammatory signaling. Ligand binding induces heterodimerization with IL1RAP and recruitment of MYD88, IRAK1/4, and TRAF6. This triggers activation of NF-??B and MAPK pathways, leading to AP-1-mediated transcription of IL-6, TNF-??, and other cytokines. The pathway is naturally balanced by IL-1RA. Disruption of IL1R1 in this model blocks the upstream receptor, providing a clean genetic system to study IL-1-dependent signaling cascades and downstream effector functions.

In lung carcinoma, IL-1R1 signaling promotes tumor-promoting inflammation, enhancing proliferation, survival, migration, and immune evasion. This knockout model allows dissection of tumor-intrinsic IL-1 responses from microenvironmental contributions, offering insights into how loss of IL-1R1 rewires signaling networks and alters the cytokine milieu. It is especially valuable for evaluating the role of IL-1 in driving oncogenic processes and for testing hypotheses about IL-1-targeted therapies in squamous cell lung cancer.

Applications include inflammation research, cancer immunology, drug target validation, and signal transduction studies. Representative assays with these cells involve western blotting for NF-??B and MAPK activation, RT-qPCR or ELISA for IL-6 and TNF-??, NF-??B reporter assays, and functional tests like proliferation, migration, and invasion. The polyclonal population can also serve as a platform for screening IL-1 pathway inhibitors or studying compensatory pathways. For further details or to discuss customization, please contact Ascent Research.

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