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Cat. No. ARG35625

IL11 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

IL11 Knockout A-549 Polyclonal Cells is a CRISPR/Cas9-edited polyclonal knockout population in human lung carcinoma epithelial (A-549) cells, engineered to disrupt the IL11 gene. This model eliminates IL11 cytokine production, interrupting JAK/STAT3 signaling and downstream targets including cyclin D1 and COL1A1. It is ideal for investigating IL11??s role in lung cancer progression, fibrosis, and STAT3-dependent gene regulation, using assays such as western blotting, proliferation, and drug screening. The polyclonal format offers a genetically diverse pool for robust functional studies.

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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

    IL11

    Gene Identifier

    NCBI Gene ID 3589

    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

IL11 Knockout A-549 Polyclonal Cells is a CRISPR/Cas9-edited polyclonal knockout cell population providing loss-of-function of the IL11 gene in human A-549 cells. The polyclonal nature ensures a heterogeneous mix of cells with diverse IL11-disruptive mutations, offering a convenient and biologically varied model without clonal selection constraints. This product enables robust investigation of IL11-dependent processes in lung epithelial biology.

The A-549 host line is a hypotriploid human lung carcinoma epithelial cell model derived from a 58-year-old Caucasian male. It is widely employed as an in vitro surrogate for alveolar type II pneumocytes, retaining key epithelial traits and responsiveness to cytokines. Thus, it is well-suited for studying lung cancer pathophysiology and pulmonary fibrosis in a human epithelial context.

IL11 encodes a pleiotropic cytokine that signals through the IL11RA/gp130 receptor to activate JAK1/JAK2 and STAT3, with downstream targets including cyclin D1, c-MYC, BCL2, and pro-fibrotic genes COL1A1 and fibronectin. Upstream regulators such as TGF-??, IL-1??, and TNF-?? drive IL11 expression via NF-??B and AP-1. IL11 also engages the PI3K-AKT and MAPK/ERK pathways. Negative feedback is mediated by SOCS3. Disruption of IL11 in these cells therefore impedes JAK/STAT3 signaling, impairing the expression of proliferation, survival, and fibrosis-associated genes.

In A-549 cells, IL11 knockout abrogates autocrine cytokine loops that drive malignant and fibrotic phenotypes. This model is invaluable for dissecting IL11’s role in lung cancer cell proliferation, migration, and apoptosis, as well as its contribution to epithelial-mesenchymal transition through SNAI1 and TWIST. Moreover, it provides a platform to study IL11-mediated pulmonary fibrosis signaling in alveolar epithelial cells and permits analysis of paracrine effects in the tumor microenvironment.

Key applications include western blotting for IL11 and phospho-STAT3, RT-qPCR for target genes, and functional assays such as MTT, scratch wound, and Annexin V staining. The polyclonal knockout pool is also appropriate for RNA-seq, drug screening with JAK/STAT inhibitors, and xenograft tumor models. Co-culture systems can recapitulate epithelial-fibroblast interactions. For further information, please contact Ascent Research.

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