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Cat. No. ARG34545

IL4 Knockout ACHN Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Pleural effusion

  • Disease:

    Papillary renal cell carcinoma

The IL4 Knockout ACHN Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the ACHN human renal adenocarcinoma cell line, with targeted disruption of the IL4 gene. IL-4 is a Th2 cytokine that signals via the IL4RA/IL2RG receptor complex and JAK1/JAK3 kinases to activate STAT6, which transcriptionally regulates type 2 immunity and IgE class switching. This loss-of-function model enables detailed studies of IL-4/STAT6 signaling in renal cell carcinoma, including tumor-intrinsic effects, immune microenvironment modulation, and drug response. Key applications encompass western blotting for phospho-STAT6, ELISA, co-culture assays with B cells, and screening of JAK/STAT inhibitors.

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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

    IL4

    Gene Identifier

    NCBI Gene ID 3565

    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 IL4 Knockout ACHN Polyclonal Cells provide a CRISPR/Cas9-mediated loss-of-function model for the human IL4 gene in the ACHN renal adenocarcinoma cell background. Delivered as a polyclonal knockout cell population, these cells have undergone CRISPR/Cas9-mediated gene disruption without single-cell cloning, preserving population heterogeneity while eliminating IL-4 expression. This model enables dissection of IL-4-dependent signaling in a metastatic renal cell carcinoma (RCC) context.

The ACHN cell line was established from a malignant pleural effusion of a 22-year-old male with metastatic renal adenocarcinoma. It serves as a widely used in vitro model for renal cell carcinoma research, displaying aggressive characteristics including rapid proliferation and high invasiveness, and is extensively applied in tumor biology and therapeutic development studies.

Interleukin-4 (IL-4) is a key Th2 cytokine that exerts its effects by binding to a heterodimeric receptor composed of IL4R?? (IL4RA) and either the common gamma chain (IL2RG) or IL13RA1. Ligand engagement activates receptor-associated Janus kinases JAK1 and JAK3, which phosphorylate the latent transcription factor STAT6. Phosphorylated STAT6 homodimerizes and translocates to the nucleus to induce expression of target genes involved in Th2 differentiation, B cell class switching to IgE, and upregulation of cell surface molecules such as MHC II and CD23. The signaling cascade is subject to negative regulation by SOCS1 and is initiated by upstream signals including T cell receptor activation, IL-2 stimulation, and the transcription factors NFAT and GATA3, creating an autocrine loop that reinforces IL-4 production.

In the context of renal cell carcinoma, IL-4 signaling has been associated with modulation of tumor cell behavior and the immune landscape. ACHN cells endogenously express IL-4 receptor subunits and can respond to IL-4 stimulation with altered proliferative and secretory profiles. By abrogating IL-4 expression, the knockout model enables researchers to dissect tumor-intrinsic versus microenvironmental contributions of IL-4, particularly regarding immune cell recruitment, polarization, and resistance to checkpoint blockade. This system is thus instrumental for exploring IL-4 as a therapeutic target in RCC.

The IL4 Knockout ACHN Polyclonal Cells support a broad range of functional assays, including Western blotting for phosphorylated STAT6, ELISA-based measurement of IL-4 and IgE, quantitative RT-PCR profiling of STAT6-dependent genes, flow cytometric analysis of CD23 expression, and co-culture experiments with B lymphocytes to monitor IgE class switching. Additional applications encompass cell migration and invasion assays, high-throughput screening of JAK/STAT pathway inhibitors, and global transcriptomic analyses via RNA sequencing. For detailed technical specifications or ordering inquiries, please contact Ascent Research.

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