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Cat. No. ARG40479

EDIL3 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The EDIL3 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from human A-549 lung adenocarcinoma epithelial cells, with targeted disruption of the EDIL3 gene. EDIL3 encodes an integrin ligand that activates FAK/PI3K/AKT and MAPK/ERK pathways, promoting cell survival and migration. This model leverages the A-549 alveolar type II-like background to study EDIL3 functions in lung cancer. Suitable for cell adhesion, migration, and apoptosis assays, these cells enable investigation of EDIL3-mediated signaling through integrins ??v??3/??v??5, and its roles in angiogenesis and efferocytosis. They serve as a valuable tool for cancer biology, drug screening, and inflammation research.

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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

    EDIL3

    Gene Identifier

    NCBI Gene ID 10085

    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

The EDIL3 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung adenocarcinoma cell line, generated for targeted disruption of the EDIL3 gene. This loss-of-function model, produced without clonal selection, provides a heterogeneous pool of edited alleles suitable for bulk functional analyses of EDIL3-dependent cellular processes.

A-549 cells serve as a classical alveolar type II-like lung adenocarcinoma model, extensively characterized for studies of epithelial biology, oncogenic transformation, and drug response. Their well-defined signaling networks and reproducible growth characteristics render them a dependable host for knockout generation, ensuring consistent experimental outcomes across replicate experiments.

Upon integrin engagement, EDIL3 promotes focal adhesion formation and activates FAK and Src, which phosphorylate downstream effectors including PI3K and the MAPK pathway. This leads to AKT and ERK1/2 phosphorylation, driving cell survival and proliferation. Additionally, EDIL3 enhances NF-??B activity, leading to MMP2/MMP9 expression and Bcl-2 upregulation. The gene is transcriptionally regulated by HIF-1?? under hypoxic conditions, and by inflammatory cytokines TNF-?? and IL-1??, as well as VEGF. EDIL3 also facilitates efferocytosis through phosphatidylserine recognition and interactions with BAI1 and TIM4.

In the A-549 adenocarcinoma context, EDIL3 loss impedes key oncogenic signals, making this model valuable for studying lung tumor cell adhesion, invasiveness, and survival. It enables the examination of EDIL3??s role in PI3K/AKT and MAPK/ERK pathway activation, and how its absence affects angiogenic factor secretion and inflammatory responses. This can uncover novel vulnerabilities in EDIL3-expressing lung cancers.

Researchers can employ these cells in cell adhesion assays on integrin ligands, transwell migration and invasion studies, and quantification of phosphorylated FAK by ELISA. Western blotting for phospho-AKT and phospho-ERK, immunofluorescence for integrin ??v??3 localization, and apoptosis detection by flow cytometry are also facilitated. Functional angiogenesis can be assessed via tube formation assays. These polyclonal knockout cells are ideal for drug sensitivity screening, functional genomics, and studies of efferocytosis and inflammation. For technical assistance, contact Ascent Research.

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