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Cat. No. ARG40512

EEA1 Knockout NCI-H1299 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Carcinoma

CRISPR/Cas9-edited EEA1 knockout in NCI-H1299 polyclonal cells disrupts the gene encoding an early endosome tethering protein. EEA1 functions as a Rab5 effector and PI3P-binding factor essential for endosome fusion and trafficking of internalized receptors such as EGFR, with its loss impairing receptor degradation and prolonging signaling. Derived from p53-null metastatic lung cancer cells, this model enables studies of endocytic dysfunction in cancer and drug delivery. Representative assays include transferrin uptake, EGFR degradation kinetics, and confocal immunofluorescence colocalization.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    NCI-H1299

    Sex of Donor

    Male

    Age

    43 years

    Gene Name

    EEA1

    Gene Identifier

    NCBI Gene ID 8411

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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 EEA1 Knockout NCI-H1299 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal population with disrupted EEA1 gene, providing a loss-of-function model for studying early endosome biology. Derived from the NCI-H1299 human non-small cell lung cancer line, these polyclonal knockout cells offer a genetically heterogeneous editing pool to avoid clonal artifacts while enabling functional analyses of endocytic trafficking.

The NCI-H1299 host cell line originates from a lymph node metastasis of lung carcinoma and is a widely used model for metastatic NSCLC. These cells are null for the tumor suppressor p53, a common alteration in advanced NSCLC associated with genomic instability and apoptosis resistance. Its mesenchymal and invasive properties render NCI-H1299 suitable for evaluating how endosomal perturbations influence cancer cell motility and signal transduction.

EEA1 is a Rab5 effector that specifically binds PI3P on early endosomes, tethering them to promote homotypic fusion and maturation. Activated by Rab5 and PI3K signaling, EEA1 interacts with NSF, syntaxin 13, and SNARE complexes to drive endocytic sorting. It critically governs the trafficking of internalized EGFR, determining its recycling or lysosomal degradation, and thus controls the strength and duration of downstream growth factor signals.

In p53-null NCI-H1299 NSCLC cells, loss of EEA1 disrupts early endosome fusion, impairing EGFR degradation and sustaining pro-survival signaling. This mirrors endocytic dysfunction in many cancers, where altered receptor trafficking contributes to proliferation and drug resistance. The knockout model allows dissection of how spatial signal termination affects tumorigenic properties and enables exploration of endosomal components as therapeutic targets in lung cancer.

The polyclonal knockout product suits studies on endocytic trafficking, receptor kinase downregulation, and intracellular drug delivery. Assays include transferrin uptake, EGFR degradation kinetics by western blot, EEA1 colocalization by confocal microscopy, and co-immunoprecipitation of Rab5/SNARE complexes. It also supports high-content screening for modulators of endosomal sorting. For additional details, contact Ascent Research.

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