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Cat. No. ARG42972

CCDC167 Knockout HEK293T Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Kidney

The CCDC167 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population in human HEK293T cells, enabling loss-of-function studies of CCDC167, a coiled-coil protein implicated in mitotic spindle assembly and microtubule dynamics. This model leverages the HEK293T background, known for high transfectability and robust protein expression, to investigate CCDC167's role in cell division. CCDC167 is linked to key mitotic regulators, including Aurora kinase A and PLK1, and its disruption is anticipated to cause spindle defects and mitotic arrest. The knockout cells support applications such as immunofluorescence for spindle analysis, flow cytometry for cell cycle profiling, and cancer target validation assays.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HEK293T

    Sex of Donor

    Female

    Age

    Fetus

    Derived From Site

    Fetal kidney

    Gene Name

    CCDC167

    Gene Identifier

    NCBI Gene ID 154467

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM

    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 CCDC167 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for targeted disruption of the CCDC167 gene in human HEK293T cells. This loss-of-function model facilitates investigation of CCDC167 function in mitotic spindle assembly and microtubule dynamics. The polyclonal format provides a heterogeneous genetically edited pool, ideal for pooled phenotypic screening and functional assays where clonal homogeneity is not essential.

HEK293T is a human embryonic kidney epithelial cell line transformed with adenovirus type 5 DNA and stably expressing the SV40 large T antigen. This genetic background permits episomal replication of plasmids containing the SV40 origin, leading to high-level recombinant protein expression and efficient lentiviral/retroviral particle production. The cells are highly transfectable and widely employed as a versatile platform for studying protein function, signal transduction, and viral packaging, offering an optimal host for gene-edited models.

CCDC167 encodes a coiled-coil domain-containing protein with a proposed role in mitotic progression and microtubule organization. It may be transcriptionally regulated by E2F factors and functionally interact with microtubule-associated proteins (MAPs) to modulate spindle architecture. CCDC167 is capable of self-dimerization and is linked to a mitotic regulatory network that includes Aurora kinase A, polo-like kinase 1 (PLK1), BUBR1, CDC20, and TPX2. CRISPR/Cas9-mediated disruption of CCDC167 is expected to compromise spindle assembly and chromosome segregation, likely resulting in mitotic arrest and cytokinesis failure.

Utilizing HEK293T as the host cell line offers distinct advantages for studying CCDC167 knockout phenotypes. The rapid proliferation rate and ease of cell cycle synchronization enable precise manipulation and analysis of mitotic stages. Furthermore, the robust protein expression machinery of HEK293T cells supports rescue experiments and structure-function analyses of CCDC167 domains. Given the putative oncogenic function of CCDC167, this model serves as a valuable tool for cancer biology research, including target validation and assessment of mitotic checkpoint vulnerabilities.

This polyclonal knockout cell product is amenable to diverse experimental workflows. Users can perform Western blotting to verify CCDC167 ablation and detect mitotic markers, RT-qPCR for transcript quantification, and immunofluorescence with anti-??-tubulin to visualize spindle morphology. Flow cytometry enables cell cycle distribution and Annexin V apoptosis analyses, while proliferation assays gauge growth defects. Co-immunoprecipitation can be employed to examine protein interactions with CCDC167. Such assays position this model for mechanistic studies in cell cycle regulation, cancer cell biology, and drug target identification. For product inquiries or technical support, please contact Ascent Research.

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