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Cat. No. ARG37097

IL13RA1 Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

The IL13RA1 Knockout HAP1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population disrupting IL13RA1 in the human near-haploid HAP1 cell line. IL13RA1 encodes the IL-13 receptor ??1 subunit, which pairs with IL4RA to activate JAK1/STAT6 signaling, driving expression of CCL11 and other Th2 mediators. This model is ideal for allergic disease research, IL-13 pathway dissection, and drug target validation. Applications include STAT6 phosphorylation assays, chemokine profiling, and genetic screens in a simplified genetic background. 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

    HAP1

    Sex of Donor

    Male

    Age

    40 years

    Derived From Site

    Bone marrow

    Gene Name

    IL13RA1

    Gene Identifier

    NCBI Gene ID 3597

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    IMDM

    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 IL13RA1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting IL13RA1 in the human near-haploid HAP1 cell line. This loss-of-function model enables investigation of IL13RA1-mediated signaling without clonal expansion, offering a heterogeneous pool suitable for pooled functional screens and bulk analyses. These cells support research into interleukin-13 (IL-13) and interleukin-4 (IL-4) receptor biology, allergic inflammation, and Th2-driven diseases.

The HAP1 line is a near-haploid human cell model derived from KBM-7 chronic myeloid leukemia cells, with a stable near-haploid karyotype and fibroblastoid morphology. Its single gene copy for most loci reduces genetic redundancy, making it ideal for knockout studies and genetic screens. HAP1 cells are widely used in CRISPR-based functional genomics, drug target validation, and signaling network dissection due to their ease of culture and manipulation.

IL13RA1 encodes the IL-13 receptor ??1 subunit, a critical component of the type II IL-4 receptor. Upon IL-13 or IL-4 binding, it heterodimerizes with IL4RA, activating JAK1 and TYK2 kinases that phosphorylate STAT6. Phosphorylated STAT6 dimerizes, translocates to the nucleus, and induces transcription of CCL11 (eotaxin), CCL17, CCL22, and genes driving IgE class switching. The decoy receptor IL-13R??2 also modulates ligand availability. Thus, IL13RA1 centrally mediates STAT6-dependent transcriptional programs downstream of IL-13/IL-4 in Th2 immune responses.

Disrupting IL13RA1 in the near-haploid HAP1 background creates a clear loss-of-function model, abolishing ligand-induced STAT6 phosphorylation and downstream gene expression without allele compensation. This polyclonal pool is well-suited for pooled modifier screens to identify regulators of the IL-13 pathway or assess drug specificity. Comparative studies with wild-type HAP1 cells allow validation of small molecules or antibodies targeting the IL-13/IL-4 axis, and analysis of receptor internalization and signaling cross-talk in a simplified genetic context.

Applications include allergic disease modeling (asthma, atopic dermatitis), oncology (glioblastoma, colorectal cancer), and drug target validation. Representative assays encompass phospho-STAT6 flow cytometry post-IL-13 stimulation, RT-qPCR for CCL11/CCL17/CCL22, western blotting for IL13RA1, and STAT6 reporter assays. These cells support genetic screens for pathway modulators and cytokine response profiling. For additional technical details or custom gene-editing services, please contact Ascent Research.

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