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Cat. No. ARG38791

DIS3L Knockout K562 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Pleural effusion

  • Disease:

    Chronic myeloid leukemia

The DIS3L Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the DIS3L gene in the HeLa cervical adenocarcinoma cell line. DIS3L is the catalytic 3'-5' exoribonuclease subunit of the RNA exosome, interacting with factors like EXOSC2, EXOSC3, SKIV2L2, and ZCCHC8 to process and degrade unstable mRNAs, non-coding RNAs, and rRNA precursors. This loss-of-function model enables investigation of RNA degradation and surveillance pathways, making it valuable for cancer biology and drug target validation. Applications include RNA-seq analysis, RNA stability assays, and cellular proliferation or apoptosis assays to study DIS3L-dependent RNA homeostasis.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    K562

    Sex of Donor

    Female

    Derived From Site

    In situ; Pleural effusion

    Gene Name

    DIS3L

    Gene Identifier

    NCBI Gene ID 115752

    Growth Mode

    Suspension

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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 DIS3L Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the DIS3L gene has been disrupted to generate a loss-of-function model for studying RNA exosome-mediated surveillance and degradation. This polyclonal knockout pool provides a heterogeneous cell population with targeted disruption of DIS3L, enabling functional studies in a human cervical adenocarcinoma background. The product is intended for researchers investigating the molecular roles of DIS3L in RNA processing and homeostasis.

The host cell line, HeLa, is an HPV18-positive cervical adenocarcinoma cell line widely employed as a model system in cancer biology and molecular cell biology. Originally derived from a cervical tumor, HeLa cells offer a robust platform for examining gene function due to their well-characterized genome, ease of culture, and responsiveness to genetic manipulation. Their epithelial origin and tumorigenic properties make them particularly useful for exploring the intersection of RNA metabolism and cancer pathogenesis.

DIS3L encodes the catalytic subunit of the RNA exosome, exhibiting 3′-5′ exoribonuclease activity essential for the processing and degradation of diverse RNA substrates, including mRNA, rRNA, and non-coding RNAs. Within the exosome complex, DIS3L interacts with core subunits such as EXOSC2 and EXOSC3, and its activity is coordinated by cofactors including the SKIV2L2 (Mtr4) helicase, ZCCHC8, and the NEXT (nuclear exosome targeting) complex. DIS3L functions in key pathways like RNA degradation and surveillance, where it targets unstable mRNAs, non-coding RNAs, and rRNA precursors. Disruption of DIS3L leads to accumulation of exosome substrates, perturbing RNA homeostasis.

In the HeLa cellular context, abrogation of DIS3L activity provides a powerful model to dissect the consequences of impaired RNA decay on cancer cell biology. The accumulation of aberrant RNA species can trigger stress responses and affect processes such as cell proliferation and viability, which are highly relevant to cervical carcinoma. This knockout model allows for the systematic evaluation of RNA exosome function in a cancer-relevant setting, facilitating the identification of downstream targets and interacting factors that mediate DIS3L??s biological effects.

Researchers can utilize this polyclonal knockout cell population in a variety of experimental workflows, including RNA-seq to profile global transcriptomic changes, RNA stability assays to measure decay kinetics, and RT-qPCR or northern blotting to validate specific transcript alterations. Functional assays such as MTT or colony formation assays can assess proliferation, while flow cytometry and apoptosis assays provide insights into cell fate decisions. For further details and technical support, please contact Ascent Research.

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