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Cat. No. ARG37646

BET1 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

BET1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from HeLa cells, featuring targeted disruption of the BET1 gene. BET1 functions as a Qb-SNARE within the ER-Golgi SNARE complex, interacting with STX5, GOSR1, and SEC22B to facilitate COPII vesicle tethering and fusion, thus executing anterograde cargo transport. This model provides a valuable system for investigating secretory pathway dynamics, cancer cell biology, and protein trafficking disorders in an HPV18-positive cervical adenocarcinoma background. Typical applications include VSVG transport kinetics, co-immunoprecipitation of SNARE partners, and immunofluorescence-based Golgi morphology assessment.

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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

    BET1

    Gene Identifier

    NCBI Gene ID 10282

    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 BET1 Knockout HeLa Polyclonal Cells are a population of HeLa cells subjected to CRISPR/Cas9-mediated disruption of the BET1 gene, generating a heterogeneous pool with reduced BET1 function. This polyclonal knockout model facilitates population-based studies of ER-Golgi SNARE-dependent trafficking without the biases of single-cell cloning. BET1 encodes a Qb-SNARE essential for COPII vesicle tethering and fusion, making this product a valuable tool for dissecting anterograde transport mechanisms.

The HeLa host cell line originates from HPV18-positive cervical adenocarcinoma and is a widely used epithelial cancer model with robust, characterized secretory pathway activity. Its tumor-derived background and genetic tractability make it particularly suitable for investigating the interplay between oncogenesis and membrane trafficking. HeLa cells provide a consistent platform for analyzing the role of BET1 in maintaining Golgi organization and secretory flux in a cancer context.

BET1 forms a core SNARE complex with STX5, GOSR1, SEC22B, and BNIP1, which specifically drives the docking and fusion of COPII vesicles??coated by SEC23/SEC24, SEC13/SEC31, and activated by SAR1??with the cis-Golgi. This function is subject to upstream regulation by ER stress signals and cell cycle machinery, while downstream consequences include modulation of Golgi integrity and secretory pathway throughput. Loss of BET1 disrupts this coordinated interaction, providing a direct means to probe SNARE assembly and cargo delivery.

In the HeLa context, BET1 knockout addresses the increased reliance of cancer cells on efficient secretion for growth factor receptor delivery and extracellular matrix remodeling. The HPV18-positive status further invites exploration of viral manipulation of host trafficking pathways. By uncoupling COPII tethering from Golgi membrane fusion, researchers can study adaptive responses to ER-Golgi transport stress and identify vulnerabilities in the secretory infrastructure of tumor cells.

Key applications include western blotting and immunofluorescence for assessing BET1 expression and Golgi morphology, co-immunoprecipitation to analyze SNARE complex formation, and the VSVG-ts045 assay to track ER-to-Golgi transport kinetics. Secretion assays and RNAi rescue experiments further enable functional validation. These polyclonal knockout cells are ideally suited for investigations in cancer cell biology, secretory pathway dynamics, and host-pathogen interactions. For additional information, please contact Ascent Research.

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