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Cat. No. ARG40009

DUS3L Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

The DUS3L Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population in the near-haploid HAP1 chronic myeloid leukemia line, featuring targeted disruption of the dual-specificity phosphatase DUS3L. This loss-of-function model aids in dissecting negative regulation of the MAPK/ERK cascade, where DUS3L dephosphorylates activated ERK1/2 downstream of RTK/RAS/RAF/MEK signaling. The polyclonal pool is ideal for functional genomics, drug sensitivity profiling, and synthetic lethality screens in leukemia research, with typical assays including phospho-ERK Western blotting and cell viability assessment. Contact Ascent Research for more information.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HAP1

    Sex of Donor

    Male

    Age

    40 years

    Derived From Site

    Bone marrow

    Gene Name

    DUS3L

    Gene Identifier

    NCBI Gene ID 56931

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    IMDM

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% COâ‚‚

  • 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. It 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 HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human near-haploid HAP1 cell line. This product contains a heterogeneous pool of cells with targeted disruption of the DUS3L gene, providing a loss-of-function model suitable for functional studies. The polyclonal format preserves genetic diversity while ensuring effective gene knockout across the population, facilitating pooled assays and pharmacological evaluations.

HAP1 is a near-haploid chronic myeloid leukemia (CML) cell line originally derived from the KBM-7 line, harboring the BCR-ABL1 fusion oncogene. Its adherent fibroblast-like morphology and near-haploid karyotype make it ideal for recessive genetic screens, as only one allele per gene needs inactivation. This characteristic enables efficient dissection of oncogenic signaling and identification of synthetic lethal interactions in leukemia models.

DUS3L encodes an atypical dual-specificity phosphatase that negatively regulates MAPK signaling by dephosphorylating tyrosine and threonine residues on activated ERK1/2 (MAPK1/3). Acting downstream of RTK/RAS/RAF/MEK/ERK signaling, DUS3L is regulated by mitogenic stimuli and reactive oxygen species, and may interact with scaffolding proteins. By attenuating ERK1/2 phosphorylation, DUS3L dampens transcriptional responses and proliferation signals, serving as a key control point in tyrosine kinase cascades.

In HAP1 cells with BCR-ABL1-driven MAPK activation, DUS3L knockout amplifies ERK1/2 phosphorylation and proliferative signaling, potentially revealing vulnerabilities in kinase inhibitor sensitivity. The near-haploid background ensures complete gene disruption, enabling clear phenotypic analyses of DUS3L??s role in leukemia cell growth, survival, and drug response. This model is valuable for exploring feedback regulation in oncogenic MAPK signaling.

This knockout cell pool supports functional genomics screens, synthetic lethality studies, and MAPK pathway dissection using assays such as phospho-ERK Western blotting, RT-qPCR, MTT viability assays, flow cytometry, and colony formation. The polyclonal format is well-suited for pooled CRISPR screens and dose?Cresponse experiments with kinase inhibitors. For further details and ordering, contact Ascent Research.

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