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Cat. No. ARG40191

DYNLT3 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

DYNLT3 Knockout HeLa Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population targeting the DYNLT3 gene in the HeLa background. DYNLT3 encodes a dynein light chain that governs intracellular transport, mitotic spindle assembly, and apoptotic signaling through interactions with dynein subunits, Bcl-2, and Bim. This knockout model is suitable for applications such as western blotting, immunofluorescence, flow cytometry, co-immunoprecipitation, and live-cell imaging to study dynein-dependent processes in cancer and cell cycle control. The polyclonal format provides a heterogeneous loss-of-function tool for robust functional analyses. For further information, contact Ascent Research.

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Shipping Info:

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

    DYNLT3

    Gene Identifier

    NCBI Gene ID 6990

    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 DYNLT3 Knockout HeLa Polyclonal Cells are a polyclonal cell population generated by CRISPR/Cas9-mediated disruption of the DYNLT3 gene in HeLa cells. This loss-of-function model enables investigation of DYNLT3, a dynein light chain involved in intracellular transport, mitotic spindle assembly, and apoptotic signaling, within a widely used human cervical cancer cell background. The polyclonal format ensures a heterogeneous gene knockout, reflecting natural variation in editing outcomes.

HeLa cells are an HPV18-positive immortalized epithelial cell line derived from cervical adenocarcinoma. They provide a robust platform for studying cancer cell biology, cell cycle control, and cytoskeletal dynamics, making them ideal for examining the functional roles of DYNLT3 in processes often dysregulated in malignancy.

DYNLT3 facilitates cargo binding and regulates cytoplasmic dynein motor activity. It interacts with core dynein subunits DYNC1H1 and DYNC1I1, the dynactin subunit DCTN1, and mitotic regulators Ndel1 and Lis1. DYNLT3 also binds Bcl-2 and Bim, linking dynein function to apoptosis. Upstream, its expression is regulated by E2F transcription factors and CDK1, while downstream it influences spindle assembly factors and apoptotic effectors. Consequently, DYNLT3 knockout disrupts intracellular trafficking, impairs mitotic spindle organization, and alters apoptotic responsiveness, providing a comprehensive loss-of-function model for dissecting these interconnected pathways.

In HeLa cells, DYNLT3 depletion is expected to compromise mitotic fidelity, leading to chromosome segregation errors and cell cycle delays, given the reliance of these rapidly dividing cancer cells on intact spindle machinery. Moreover, disruption of DYNLT3?CBcl-2 interactions may sensitize cells to apoptotic stimuli, offering a system to explore vulnerabilities in cervical cancer and to evaluate therapeutic strategies targeting dynein-dependent processes.

This knockout model is suitable for a variety of assays, including western blotting, immunofluorescence, flow cytometry for cell cycle and apoptosis analysis, and co-immunoprecipitation to assess protein interactions. Live-cell imaging of intracellular transport and motility assays further enable functional studies. Applications span dynein biology, mitotic regulation, and cancer cell research, supporting both mechanistic investigations and drug discovery. For further details, please contact Ascent Research.

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