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Cat. No. ARG43365

CD109 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The CD109 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the CD109 gene in A-549 human lung adenocarcinoma cells. CD109 negatively regulates TGF-?? signaling by promoting degradation of TGF-?? receptors (T??RI/T??RII), modulating Smad2/3 phosphorylation and downstream effectors like AKT and ERK1/2. These knockout cells enable investigation of TGF-?? pathway dynamics, tumor progression, and drug resistance, with applications in functional genomics and therapeutic target evaluation. Representative assays include phospho-Smad Western blotting, migration/invasion assays, and co-immunoprecipitation.

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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

    CD109

    Gene Identifier

    NCBI Gene ID 135228

    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 CD109 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of the CD109 gene in the A-549 human lung adenocarcinoma epithelial cell line. This product provides a heterogeneous pool of edited cells suitable for immediate functional studies without clonal isolation, enabling robust analysis of CD109-mediated regulation.

The A-549 cell line is a widely utilized model in cancer biology and drug testing, derived from human lung adenocarcinoma. Its epithelial origin and intact TGF-?? signaling machinery make it an ideal host for investigating the consequences of CD109 loss in a physiologically relevant tumor context. A-549 cells are commonly employed to study signaling pathways, proliferation, and metastasis.

CD109 is a GPI-anchored glycoprotein that negatively regulates TGF-?? signaling by binding to TGF-?? receptors (T??RI and T??RII) and promoting their internalization and degradation via caveolae-mediated endocytosis, a process involving interactions with caveolin-1, Smad7, and E3 ubiquitin ligases. This attenuates phosphorylation of Smad2/3 and downstream transcriptional responses. CD109 expression is induced by TGF-??1, TGF-??2, EGF, hypoxia, and STAT3, and its activity further modulates AKT and ERK1/2 phosphorylation, MMP expression, and EMT markers. Thus, CD109 integrates signals from TGF-??/Smad, JAK/STAT, PI3K/AKT, and MAPK/ERK pathways.

In A-549 lung adenocarcinoma cells, CD109 knockout serves as a critical tool to dissect TGF-?? pathway dynamics, particularly in the context of tumor progression where TGF-?? switches from tumor-suppressive to pro-metastatic. The polyclonal knockout population allows examination of enhanced TGF-?? signaling on proliferation, migration, invasion, and EMT, and facilitates investigation of CD109 as a potential therapeutic target in non-small cell lung cancer and other malignancies.

Key applications include Western blotting for Smad2/3 phosphorylation, TGF-??-responsive luciferase reporter assays, RT-qPCR of target genes, immunofluorescence for receptor localization, co-immunoprecipitation of CD109 with T??RI/T??RII, and functional migration/invasion assays. Flow cytometry can assess CD109 surface expression. These cells support drug resistance studies, functional genomics screens, and target validation. For technical inquiries, contact Ascent Research.

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