Quick Order Cart

Cat. No. ARG31896

ATRX Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

ATRX Knockout A-549 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population in the A-549 human lung adenocarcinoma cell line, with targeted disruption of the ATRX chromatin remodeler. Loss of ATRX, which normally cooperates with DAXX to deposit H3.3 at telomeres, triggers alternative lengthening of telomeres (ALT) and transcriptomic alteration, contributing to oncogenic progression. This model is suited for ALT research, telomere biology, chromatin studies, and ATR inhibitor drug screening. Key interacting factors include DAXX, H3.3, ATM, and ATR, making these cells a powerful tool for investigating the molecular consequences of ATRX deficiency in lung cancer.

Inquire Now

In stock

Ships next business day


Ask a Question

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

    ATRX

    Gene Identifier

    NCBI Gene ID 546

    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 ATRX Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population of human origin, derived from the A-549 lung adenocarcinoma epithelial cell line, with targeted disruption of the ATRX gene. This heterogeneous pool ensures robust ATRX inactivation across the population, providing a versatile tool for investigating ATRX loss-of-function in cancer biology.

The A-549 cell line, established from a human non-small cell lung carcinoma, serves as a classic model for studying lung adenocarcinoma. These adherent epithelial cells are employed in research on barrier integrity, xenobiotic metabolism, and oncogenic signaling. Their widespread use in cancer studies facilitates the translation of ATRX knockout findings to clinically relevant contexts.

ATRX is an SWI/SNF-family chromatin remodeler that, in a complex with the histone chaperone DAXX, deposits histone variant H3.3 into telomeric and pericentric heterochromatin. This process is critical for maintaining telomere structure and genome integrity. ATRX activity is modulated by upstream DNA damage sensors ATM and ATR, while its downstream effects include regulation of ALT pathway activation and expression of genes such as ID1 and ID3. Interacting factors like HP1, macroH2A, and cohesin further link ATRX to higher-order chromatin organization. Consequently, ATRX knockout abrogates H3.3 deposition, eliciting ALT and transcriptional reprogramming that drive tumor progression.

Introducing ATRX knockout into the A-549 background generates a powerful model to dissect the role of chromatin dysregulation in ALT and lung adenocarcinoma pathogenesis. This system is particularly suited for investigating synthetic lethal interactions with ATR inhibitors, as A549 cells harbor relevant genetic vulnerabilities. The polyclonal nature captures variable knockout efficiencies, reflecting tumor heterogeneity and enhancing the model’s utility for studying telomere maintenance and drug response mechanisms.

This product is ideal for research into ALT mechanisms, telomere biology, and chromatin dynamics, as well as for evaluating ATR inhibitor sensitivity. Representative assays include immunofluorescence detection of ALT-associated PML bodies (APBs), C-circle amplification, telomere FISH, RNA sequencing, colony formation, and drug sensitivity testing. The ATRX Knockout A-549 Polyclonal Cells offer a robust platform for cancer and telomere research. For further details, contact Ascent Research.

Reset Password

    Reach Us Questions? Click Me Here!

    Fill out the form below and a member of our team will contact you shortly!

    *Required field



      Reach Us

      Fill out the form below and a member of our team will contact you shortly!

      *Required field

      Product Inquiry (Optional)