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Cat. No. ARG34098

IFT140 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

CRISPR/Cas9-edited polyclonal IFT140 knockout A-549 cells provide a loss-of-function model derived from a human lung adenocarcinoma cell line. Disruption of IFT140, a key IFT-A complex subunit, impairs ciliogenesis and attenuates Hedgehog signaling by disrupting SMO trafficking and reducing GLI transcription factor activity. This model is suited for investigating cilia-dependent pathways in lung cancer, including TGF-beta and Wnt signaling, and for studying ciliopathy mechanisms. Applications include ciliary immunofluorescence, western blotting, RT-qPCR for GLI targets, Hedgehog reporter assays, and functional assays for migration, invasion, and proliferation. The polyclonal population enables analysis of heterogeneous gene disruption effects, reflecting variable ciliary function observed in tumors.

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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

    IFT140

    Gene Identifier

    NCBI Gene ID 9742

    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 IFT140 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung adenocarcinoma cell line. This product comprises a heterogeneous pool of cells with targeted disruption of the IFT140 gene, providing a versatile loss-of-function model for studying IFT140-dependent processes. The polyclonal format enables investigation of gene function while capturing natural variation in editing outcomes, making it suitable for initial functional screens and population-level analyses.

The A-549 cell line is a human lung adenocarcinoma model derived from a 58-year-old Caucasian male. These cells exhibit alveolar type II epithelial features and can assemble primary cilia under appropriate conditions, making them relevant for ciliary biology and cancer studies. A-549 is widely used in oncology and respiratory research, and its ability to form cilia positions it as a valuable system for studying cilia-dependent signaling in a lung cancer context.

IFT140 encodes a core subunit of the intraflagellar transport complex A (IFT-A), essential for retrograde ciliary trafficking from the tip to the base. IFT140 interacts with IFT-A components IFT122 and IFT43, the adaptor WDR19, tubulin, and the dynein-2 motor to maintain ciliary structure and function. Transcription of IFT140 is regulated by FOXJ1, RFX factors, and Notch signaling. Loss of IFT140 disrupts ciliogenesis and attenuates Hedgehog signaling by impairing SMO trafficking and ciliary GPCR localization, which reduces GLI transcription factor activity and alters target gene expression. IFT140 also intersects with TGF-beta and Wnt pathways, integrating multiple cilia-dependent signals.

In A-549 cells, IFT140 knockout impairs primary cilia formation and Hedgehog pathway output, providing a model to investigate how ciliary dysfunction influences lung cancer cell behavior. Aberrant Hedgehog signaling contributes to lung tumor progression and chemoresistance; thus, this model helps dissect the role of cilia in oncogenic signaling. TGF-beta signaling, another cilia-modulated pathway in certain contexts, can also be explored. The polyclonal population reflects heterogeneous ciliary loss, mimicking tumor heterogeneity.

Key applications include immunofluorescence-based ciliary analysis (acetylated tubulin, ARL13B), western blotting for IFT140, RT-qPCR for GLI target genes, and Hedgehog luciferase reporter assays. Functional studies of migration, invasion, and proliferation are also enabled. The model is valuable for ciliopathy research and screening modulators of cilia-dependent pathways. For further information, please contact Ascent Research.

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