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Cat. No. ARG38069

ATRX Knockout HEK293T Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Kidney

The ATRX Knockout HEK293T Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal HEK293T cell population with disrupted ATRX expression, offering a loss-of-function model for studying ??-thalassemia/mental retardation syndrome X-linked protein functions. ATRX, in complex with DAXX, deposits histone H3.3 at telomeres and heterochromatin to maintain genome stability. This model is valuable for investigating alternative lengthening of telomeres (ALT), chromatin remodeling, and DNA damage responses. Key interacting partners include HP1?? and the MRN complex. Researchers can employ these cells in C-circle assays, telomere FISH, and ChIP experiments, with applications in glioma, sarcoma, and neuroendocrine tumor research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HEK293T

    Sex of Donor

    Female

    Age

    Fetus

    Derived From Site

    Fetal kidney

    Gene Name

    ATRX

    Gene Identifier

    NCBI Gene ID 546

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM

    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 HEK293T Polyclonal Cells product is a polyclonal population of HEK293T cells with CRISPR/Cas9-mediated disruption of the ATRX gene, enabling loss-of-function studies in a telomerase-positive, immortalized human embryonic kidney background. This heterogeneous pool avoids clonal selection bias and provides a robust system for investigating population-level effects of ATRX deficiency, including chromatin remodeling and telomere maintenance defects.

HEK293T cells are an adenovirus 5-transformed human embryonic kidney epithelial line that stably expresses SV40 large T antigen, endowing them with exceptional transfectability and recombinant protein expression capacity. Widely employed for viral production and gene function analyses, their rapid growth and tractable genetics make them an ideal host for generating CRISPR-engineered knockout models to study fundamental processes such as genome stability and chromatin dynamics.

ATRX is a SWI/SNF chromatin remodeler that complexes with DAXX to deposit histone H3.3 at telomeres, pericentric heterochromatin, and repetitive loci, thereby safeguarding genomic stability by silencing aberrant recombination. ATRX deficiency abrogates H3.3 incorporation, triggering alternative lengthening of telomeres (ALT), DNA damage response activation, and altered TERRA transcription. It interacts with HP1??, the MRN complex (MRE11-RAD50-NBS1), MeCP2, and EZH2, integrating signals from upstream kinases ATM/ATR to regulate chromatin compaction and telomere structure.

In the telomerase-positive HEK293T background, ATRX removal creates a tractable model to probe the initiation of ALT-associated phenotypes, including changes in H3.3 distribution, telomeric C-circle accumulation, and sister chromatid exchange. The parental line??s high transfectability facilitates complementation and mutant rescue experiments, enabling dissection of ATRX functional domains. This isogenic system circumvents confounding passenger mutations found in ALT+ tumor lines, making it suitable for studying ATRX??s role in chromatin integrity and telomere capping.

These polyclonal knockout cells support diverse assays such as ChIP-qPCR for H3.3 and ATRX, telomere FISH, C-circle quantification, ??H2AX immunofluorescence, colony formation, and cell cycle analysis. Applications span chromatin biology, telomere research, ALT mechanism studies, and drug screening for gliomas, sarcomas, and pancreatic neuroendocrine tumors. For additional information or to inquire about custom gene editing services, please contact Ascent Research.

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