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Cat. No. ARG34498

KRT72 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The KRT72 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from human lung adenocarcinoma A-549 cells. This model targets the KRT72 gene, which encodes a type II keratin intermediate filament protein involved in cytoskeletal organization and epithelial-mesenchymal transition (EMT). KRT72 is regulated by p63, TGF-??, and EGF pathways, and interacts with FAK, Src, and keratin partner KRT71. Ideal for investigating KRT72 function in lung cancer progression, metastasis, and drug response, these cells are suitable for migration assays, phospho-signaling analysis, RNA-seq, and EMT pathway studies. The polyclonal format ensures robust loss-of-function analysis in a disease-relevant cell model.

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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

    KRT72

    Gene Identifier

    NCBI Gene ID 140807

    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 KRT72 Knockout A-549 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in the A-549 human lung adenocarcinoma cell line. This product offers a heterogeneous pool of edited cells with disruption of the KRT72 gene, achieved through CRISPR/Cas9-mediated gene targeting. The polyclonal format preserves diverse genetic backgrounds while enabling robust loss-of-function analysis of KRT72. This cell population is suitable for researchers studying keratin biology and lung cancer progression.

The A-549 host cell line is an immortalized epithelial cell line derived from a 58-year-old Caucasian male with lung adenocarcinoma. It displays adherent morphology and wild-type EGFR expression, and is widely employed as a model for human lung adenocarcinoma, particularly in studies of cancer biology, drug metabolism, and respiratory disease. The well-characterized nature of A-549 cells makes them a reliable platform for investigating gene function and therapeutic responses in non-small cell lung cancer (NSCLC).

KRT72 encodes a type II keratin intermediate filament protein that assembles into cytoskeletal networks by pairing with type I keratins such as KRT71. In epithelial cells, KRT72 is implicated in maintaining structural integrity and regulating cell motility. Its expression is governed by upstream regulators including p63, AP-1, EGF, and TGF-?? signaling, while it functionally interacts with desmosomal proteins like Desmoplakin and Plakoglobin, and modulates downstream effectors such as FAK and Src kinases. KRT72 thereby influences focal adhesion dynamics and epithelial-mesenchymal transition (EMT) programs, with potential crosstalk to E-cadherin and Vimentin expression.

In the context of A-549 lung adenocarcinoma cells, disruption of KRT72 provides a powerful tool to dissect its contributions to cancer cell migration, invasion, and cytoskeletal reorganization. Given the involvement of keratin networks in EMT??a process central to metastasis??this knockout model enables the interrogation of KRT72??s role in modulating cellular plasticity and drug sensitivity. Researchers can utilize this system to explore how loss of KRT72 affects the balance between epithelial and mesenchymal states, as well as focal adhesion signaling cascades critical for metastatic dissemination.

Typical research applications for these polyclonal knockout cells include functional studies of KRT72 in NSCLC progression, detailed analysis of EMT and metastasis mechanisms, and cytoskeletal remodeling investigations. They are compatible with a range of experimental assays such as Western blotting, RT-qPCR, immunofluorescence, Transwell migration, and wound healing assays. Moreover, these cells can be employed in global transcriptomic analyses via RNA-seq, phospho-signaling profiling to assess FAK/Src activity, and drug sensitivity screens to evaluate responses to targeted therapies. For inquiries and ordering, contact Ascent Research.

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