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Cat. No. ARG38935

DLGAP5 Knockout K562 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Pleural effusion

  • Disease:

    Chronic myeloid leukemia

CRISPR/Cas9-edited polyclonal knockout cells targeting DLGAP5 in the K-562 chronic myelogenous leukemia model. DLGAP5 (HURP) is a mitotic spindle assembly factor regulated by Ran GTPase and Aurora A kinase, stabilizing kinetochore microtubules for accurate chromosome segregation. This loss-of-function model enables investigation of spindle dynamics, genome stability, and cell cycle progression in a Philadelphia chromosome-positive leukemic background. Suitable for studies of mitotic regulation, synthetic lethality, and drug target validation. Western blotting, immunofluorescence, flow cytometry, and cell viability assays are representative readouts for characterizing DLGAP5-dependent phenotypes and therapeutic vulnerabilities.

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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

    DLGAP5

    Gene Identifier

    NCBI Gene ID 9787

    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 DLGAP5 Knockout K-562 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human K-562 lymphoblastoid leukemia cell line. This product offers a genetically disrupted DLGAP5 locus, generating a robust loss-of-function model for investigating the mitotic functions of DLGAP5 (also known as HURP). The polyclonal knockout pool minimizes artifacts associated with single-cell clonal selection, enabling functional studies of spindle assembly and cell cycle regulation in a leukemic background.

K-562 is a widely characterized cell line established from the pleural effusion of a patient with Philadelphia chromosome-positive chronic myelogenous leukemia (CML) in blast crisis. As a suspension lymphoblastoid line, K-562 serves as a standard model for CML and for studying BCR-ABL-driven oncogenic signaling, providing a clinically relevant host for dissecting mitotic vulnerabilities in leukemia.

DLGAP5 is a mitotic spindle assembly factor that stabilizes kinetochore microtubules, essential for proper chromosome alignment and segregation. The protein is recruited to spindle microtubules via a Ran GTPase-dependent mechanism and activated through Aurora A-mediated phosphorylation. Upstream regulation involves E2F transcription factors and the TPX2?CAurora A kinase module, with importin ?? further modulating localization. Downstream, DLGAP5 influences microtubule dynamics, mitotic progression, and genome stability. It functions within a core spindle regulatory network including Ran GTPase, TPX2, Aurora A, and importin ??, linking mitotic signaling to the fidelity of chromosome segregation.

In the K-562 CML background, dysregulated cell cycle control driven by the BCR-ABL oncogene creates a unique context to examine how spindle assembly defects contribute to leukemic proliferation. DLGAP5 is overexpressed in multiple malignancies??including hepatocellular carcinoma, breast cancer, and lung adenocarcinoma??and portends poor prognosis. Disruption of DLGAP5 in a leukemic model may uncover synthetic lethal interactions with oncogenic signaling or enhance sensitivity to spindle-targeting chemotherapeutics, offering a platform for translational studies.

The DLGAP5 Knockout K-562 Polyclonal Cells are designed for experimental applications such as mechanistic dissection of mitotic spindle assembly, functional analysis of chromosome segregation, identification of synthetic lethal relationships, and preclinical validation of mitotic drug targets. Recommended approaches include Western blotting to confirm DLGAP5 loss, immunofluorescence imaging of spindle morphology and chromosome alignment, flow cytometry for cell cycle distribution and apoptosis, and cell proliferation assays. For further information, please contact Ascent Research.

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