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Cat. No. ARG39976

DUS1L Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The DUS1L Knockout A-549 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population in the A-549 lung adenocarcinoma cell line, targeting the tRNA dihydrouridine synthase DUS1L. This loss-of-function model disrupts a key enzyme in tRNA modification, linking translational regulation to cancer biology. DUS1L functions downstream of MYC and mTOR signaling, and its knockout may affect translation of specific mRNAs, proliferation, and stress responses. Ideal for studying epitranscriptomic contributions to non-small cell lung cancer, these polyclonal cells enable assays such as tRNA modification profiling, proliferation analysis, and drug screening. For technical inquiries, contact Ascent 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

    DUS1L

    Gene Identifier

    NCBI Gene ID 64118

    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 DUS1L Knockout A-549 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population generated from the A-549 human lung adenocarcinoma epithelial cell line, designed for loss-of-function analysis of the DUS1L gene. This polyclonal format provides a heterogeneous disruption pool, avoiding clonal selection while maintaining a representative knockout background.

The parental A-549 cell line, originally derived from a 58-year-old Caucasian male with lung adenocarcinoma, is a well-established non-small cell lung cancer (NSCLC) model. These adherent epithelial cells retain hallmark features of NSCLC and are extensively used in oncology research for studying proliferation, drug sensitivity, and signaling pathways.

DUS1L encodes a tRNA dihydrouridine synthase responsible for catalyzing the conversion of uridine to dihydrouridine in the D-loop of tRNAs. This post-transcriptional modification is essential for tRNA structural integrity and translational fidelity. DUS1L operates downstream of mTOR signaling and is transcriptionally activated by MYC, thereby integrating growth and nutrient cues with protein synthesis. The enzyme interacts with tRNA substrates and is likely a component of the dihydrouridine synthase complex. Disruption of DUS1L can dysregulate the translation of codon-biased mRNAs and perturb the phosphorylation of key translation regulators, including S6K and eIF4E, ultimately affecting cellular stress responses and proliferation.

In the context of A-549 NSCLC cells, knockout of DUS1L offers a powerful tool to examine the contribution of tRNA modifications to oncogenic phenotypes. Loss of DUS1L may impair proliferation, heighten sensitivity to oxidative stress, and diminish tumorigenic capacity by altering translational landscapes. This model facilitates dissection of the MYC-mTOR-DUS1L axis and its role in driving malignant features of lung adenocarcinoma.

These DUS1L knockout polyclonal cells are suitable for a range of applications, including investigation of tRNA modification in cancer, translational control studies, functional genomics of lung adenocarcinoma, and drug target screening. Representative assays include western blotting for translation regulators (e.g., phospho-S6K, eIF4E), tRNA modification profiling by LC-MS, proliferation and colony formation, apoptosis, migration/invasion, and drug sensitivity testing. The polyclonal nature makes them ideal for experiments requiring a genetically diverse knockout population. For further information, please contact Ascent Research.

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