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Cat. No. ARG34434

JMJD4 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

CRISPR/Cas9-edited polyclonal knockout cell population of JMJD4 in A-549 human lung adenocarcinoma cells. This model disrupts the ribosomal protein demethylase JMJD4, which regulates RPS2 demethylation and translational control downstream of mTORC1 and MYC. It is suitable for studying lung cancer biology, ribosome biogenesis, and translation regulation. Applications include polysome profiling, RPS2 methylation analysis by Western blot, and puromycin incorporation assays. This polyclonal pool is ideal for population-level studies of JMJD4 loss-of-function in epithelial lung cancer.

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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

    JMJD4

    Gene Identifier

    NCBI Gene ID 65094

    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 JMJD4 Knockout A-549 Polyclonal Cells constitute a polyclonal knockout cell population generated through CRISPR/Cas9-mediated disruption of the JMJD4 gene in the A-549 human lung adenocarcinoma cell line. This loss-of-function model enables investigation of JMJD4-dependent cellular processes, particularly those related to ribosomal protein modification and translation control. As a polyclonal population, the product captures a range of editing events, making it well-suited for experiments requiring bulk cell analyses rather than clonal phenotypes.

A-549 is an adherent epithelial cell line derived from a non-small cell lung carcinoma patient, widely used in cancer research. These cells carry an activating KRAS mutation, reflecting a common genetic alteration in lung adenocarcinoma, and maintain alveolar basal epithelial features. Their robust growth and extensive characterization make them a practical host for generating knockout models to study lung cancer biology and therapeutic responses.

JMJD4 functions as a lysine demethylase specific for ribosomal protein RPS2, a component of the 40S subunit. Demethylation of RPS2 by JMJD4 is regulated by upstream signals, including mTORC1 and MYC, and is essential for ribosome biogenesis and efficient translation initiation. The JMJD4?CRPS2 axis interfaces with translation factors such as eIF2??, linking nutrient-sensing pathways to protein synthesis. Knockout of JMJD4 disrupts this demethylation event, potentially impairing ribosomal function and global translation.

In the A-549 context, loss of JMJD4 provides a relevant system to assess the impact of ribosomal protein methylation on lung cancer cell growth. The knockout is expected to reduce RPS2 demethylation, compromise 40S subunit activity, and attenuate protein synthesis, thereby affecting proliferation and tumorigenic potential. This model allows systematic exploration of how translational control mechanisms contribute to non-small cell lung carcinoma, and may inform strategies targeting ribosomal modifications for therapy.

This polyclonal knockout product can be used in polysome profiling to examine ribosome assembly, Western blotting to detect RPS2 methylation levels, and puromycin incorporation assays to measure translation rates. Cell proliferation assays and RNA-seq further enable phenotypic and transcriptomic analyses. Applications span lung cancer biology, ribosome biogenesis, translation regulation, epigenetic modulation, and drug target identification. For additional details or to place an order, please contact Ascent Research.

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