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Cat. No. ARG34547

IL13 Knockout ACHN Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Pleural effusion

  • Disease:

    Papillary renal cell carcinoma

The IL13 Knockout ACHN Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the ACHN renal adenocarcinoma line, with targeted disruption of IL13. This model abolishes interleukin-13 signaling through the IL4R??/IL13R??1 complex, preventing activation of JAK/STAT6 and PI3K/AKT pathways. These cells facilitate the study of IL-13 functions in renal cell carcinoma, including tumor microenvironment cytokine signaling and immune evasion. Applications include Western blotting for phospho-STAT6, RT-qPCR of downstream targets like CCL11 and SOCS1, and inhibitor screening.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    ACHN

    Sex of Donor

    Male

    Age

    22 years

    Gene Name

    IL13

    Gene Identifier

    NCBI Gene ID 3596

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM (with NEAA)

    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 IL13 Knockout ACHN Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the ACHN human renal cell adenocarcinoma line, carrying a targeted disruption of the IL13 gene. This pooled format comprises a heterogeneous mixture of edited cells, providing a cost-effective and robust loss-of-function model for investigating interleukin-13 signaling in cancer biology without requiring single-cell cloning.

The parental ACHN cell line was originally derived from the pleural effusion of a 22-year-old male patient with renal cell carcinoma and is a widely used in vitro model for renal cancer research. ACHN cells maintain key characteristics of renal adenocarcinoma, including epithelial morphology and responsiveness to cytokine stimulation, making them a relevant platform for dissecting tumor cell-autonomous signaling and interactions with the microenvironment.

IL13 encodes interleukin-13, a cytokine that signals through a receptor complex of IL4R?? and IL13R??1, activating JAK1 and JAK2 to phosphorylate STAT6, as well as engaging IRS1 to stimulate PI3K/AKT signaling. IL-13 is central to Th2-type immunity, promoting IgE class switching, mucus production, and expression of chemokines like CCL11 (eotaxin) and regulators such as SOCS1. Disruption of IL13 in these cells abolishes ligand-dependent signaling, preventing STAT6 activation and downstream transcriptional events.

In the context of renal cell carcinoma, autocrine or paracrine IL-13 signaling may contribute to tumor progression by enhancing cell proliferation, survival, and immune evasion. This ACHN knockout model permits rigorous dissection of tumor-intrinsic IL-13 functions, effectively decoupling cancer cell-derived cytokine effects from those mediated by infiltrating immune cells or stromal elements. It thus enables focused analysis of JAK/STAT6 and PI3K/AKT pathway contributions to renal cancer phenotypes.

This polyclonal knockout population is ideally suited for a variety of functional assays, including Western blotting for phospho-STAT6 and total STAT6, RT-qPCR analysis of downstream targets such as CCL11 and SOCS1, cell proliferation and invasion assays, cytokine ELISA profiling, transcriptomic studies via RNA-seq, and in vivo xenograft tumor growth experiments. Primary research applications encompass investigating IL-13’s role in renal cell carcinoma biology, screening small-molecule inhibitors of the IL-13 pathway, characterizing tumor microenvironment cytokine networks, and evaluating immune checkpoint modulation. For further technical details, batch-specific characterization data, or custom project inquiries, please contact Ascent Research.

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