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Cat. No. ARG40013

DUS3L Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The DUS3L Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the DUS3L gene in HeLa cervical adenocarcinoma cells. DUS3L encodes a dual-specificity phosphatase that dephosphorylates key MAP kinases, including ERK (MAPK1), JNK (MAPK8), and p38 (MAPK14), acting as a negative regulator of pathways responsive to growth factors and stress. This knockout model enables investigation of phosphatase-mediated control of MAPK signaling in an HPV18-positive background, supporting studies of cervical cancer biology. Typical applications include Western blotting for phospho-MAPKs, cell proliferation and apoptosis assays, and RT-qPCR for MAPK target genes.

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Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HeLa

    Sex of Donor

    Female

    Age

    31 years

    Gene Name

    DUS3L

    Gene Identifier

    NCBI Gene ID 56931

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM (with NEAA)

    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 DUS3L Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the DUS3L gene in HeLa cells. This loss-of-function model is designed to study dual-specificity phosphatase 3-like (DUS3L) function in human epithelial cells. The polyclonal nature provides a heterogeneous knockout background, minimizing clonal artifacts. The product is validated for gene disruption and is ideal for examining DUS3L-dependent MAPK signaling regulation.

HeLa cells are a HPV18-positive cervical adenocarcinoma line with inactivated p53 and Rb due to viral E6 and E7 oncoproteins. This immortalized background supports deregulated proliferation, making it a standard model for cancer signaling research. The epithelial origin and robust growth characteristics ensure consistent experimental performance across a variety of biochemical and cell-based assays.

DUS3L acts as a dual-specificity phosphatase that negatively regulates MAP kinase cascades by dephosphorylating tyrosine and serine/threonine residues on MAPK1 (ERK2), MAPK8 (JNK1), and MAPK14 (p38??). Its phosphatase domain directly interacts with these kinases to dampen signals elicited by growth factors, oxidative, and osmotic stress. Upstream receptor tyrosine kinases such as EGFR activate RAS-RAF-MEK-ERK signaling, while stress stimuli trigger JNK and p38 pathways. DUS3L-mediated attenuation is critical for controlling cell proliferation, differentiation, and stress responses.

Within HeLa cells, HPV-driven constitutive proliferative signaling renders MAPK pathway regulation particularly consequential. Loss of DUS3L likely potentiates ERK, JNK, and p38 activity, providing a tool to investigate phosphatase-dependent modulation of oncogenic and stress responses. This model is valuable for studying cervical adenocarcinoma biology and the broader role of dual-specificity phosphatases in cancer.

Researchers can employ this knockout product in Western blotting for phospho-ERK, phospho-JNK, and phospho-p38 to monitor pathway activation, in cell proliferation assays such as MTT or BrdU, and in apoptosis evaluation via Annexin V staining. RT-qPCR enables quantification of MAPK target genes, while immunofluorescence reveals subcellular kinase distribution. These applications support the elucidation of DUS3L??s regulatory functions in MAPK signaling. For further information, please contact Ascent Research.

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