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Cat. No. ARG33306

GTSE1 Knockout HT29 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

The GTSE1 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the HT29 human colorectal adenocarcinoma cell line. This model targets GTSE1, a mitotic regulator and p53 target gene that stabilizes microtubules and facilitates chromosome alignment. GTSE1 functions downstream of p53 and upstream of Aurora A, PLK1, and Cyclin B1, and interacts with BUB1 and TPX2. Knockout in HT29 cells disrupts mitotic spindle organization, enabling studies of p53 signaling, cell cycle control, and colorectal cancer progression. Ideal for flow cytometry, immunofluorescence, western blotting, and drug sensitivity profiling.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HT29

    Gene Name

    GTSE1

    Gene Identifier

    NCBI Gene ID 51512

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    McCoy's 5A

    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 GTSE1 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the HT29 human colorectal adenocarcinoma cell line. This heterogeneous pool ensures robust disruption of GTSE1 without the need for clonal isolation, maintaining genetic diversity that better mimics physiological tumor conditions. The polyclonal format is ideal for loss-of-function investigations into mitotic regulation, cell cycle control, and tumor biology.

HT29 cells are a well-established colorectal adenocarcinoma model featuring epithelial morphology and mutations in TP53 and APC, two critical tumor suppressors often inactivated in colorectal cancer. They are routinely employed to study intestinal epithelial biology, drug absorption, and oncogenic signaling pathways. Their consistent growth characteristics and defined genomic lesions make them an excellent chassis for CRISPR/Cas9-mediated gene knockout and functional genomic screens.

GTSE1 (G2 and S phase-expressed protein 1) is a downstream target of p53 that operates as a key mitotic regulator. It is transcriptionally upregulated by TP53 and FOXM1, and exerts its function by stabilizing spindle microtubules and facilitating chromosome congression. GTSE1 interacts physically with BUB1 and TPX2, linking the p53 pathway to the mitotic machinery. In the G2/M phase, GTSE1 acts upstream of Aurora A (AURKA), PLK1, Cyclin B1, and CDK1, ensuring timely mitotic entry and proper spindle assembly checkpoint function.

Within HT29 cells, which express mutant p53, knockout of GTSE1 results in severe mitotic spindle abnormalities, prolonged mitosis, and impaired cellular proliferation. These effects reveal p53-independent roles of GTSE1 in maintaining mitotic fidelity, making the model highly relevant for studying GTSE1-driven oncogenesis in colorectal cancer, where high GTSE1 levels correlate with poor clinical outcome.

This polyclonal knockout product supports a wide range of experimental approaches, including cell cycle analysis by flow cytometry, determination of mitotic index, and immunofluorescence staining for spindle markers such as ??-tubulin and pericentrin. Western blotting can assess levels of p53, cyclin B1, and other G2/M regulators. The cells are also suitable for proliferation assays (MTT, BrdU), transcriptome profiling via RNA-seq, and live-cell imaging to observe mitotic dynamics. Additionally, they serve as a platform for drug sensitivity testing and mechanistic studies of mitotic checkpoint control. For further details, please contact Ascent Research.

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