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Cat. No. ARG42965

CCDC149 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The CCDC149 Knockout HeLa Polyclonal Cells offer a CRISPR/Cas9-based loss-of-function model in human cervical adenocarcinoma cells. This heterogeneous cell population enables functional analysis of CCDC149, a coiled-coil domain-containing protein with putative roles in protein?Cprotein interactions, cytoskeletal organization, and intracellular trafficking. The HeLa background, with HPV18-driven p53 and Rb inactivation, provides a cancer-relevant context for studying this uncharacterized gene. Key applications include identification of CCDC149 interaction partners via co-immunoprecipitation, assessment of its impact on cancer cell proliferation and migration, and transcriptomic profiling. This tool is ideal for researchers exploring ciliogenesis, trafficking, or novel oncogenic mechanisms in cervical cancer models.

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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

    CCDC149

    Gene Identifier

    NCBI Gene ID 91050

    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 CCDC149 Knockout HeLa Polyclonal Cells product provides a heterogeneous population of HeLa cells with CRISPR/Cas9-mediated disruption of the CCDC149 gene, creating a polyclonal loss-of-function model. This pooled knockout format preserves genetic diversity while ensuring target gene disruption, enabling functional studies without clonal selection artifacts. The polyclonal nature offers experimental robustness, making it suitable for unbiased characterization of CCDC149 in a well-established human epithelial cell background.

The host HeLa cell line is an immortalized human cervical adenocarcinoma line (Homo sapiens, female) positive for human papillomavirus type 18 (HPV18). The viral oncoproteins E6 and E7 inactivate the tumor suppressors p53 and Rb, respectively, promoting uncontrolled proliferation and providing a widely used model for cancer biology. This genetic context makes HeLa cells particularly relevant for investigating genes potentially involved in oncogenic processes, as well as for general cell biological studies of epithelial cancers.

CCDC149 is predicted to encode a coiled-coil domain-containing protein, a structural motif known to mediate protein?Cprotein interactions, suggesting CCDC149 may function as a scaffold or adapter. While its precise molecular partners and signaling networks remain uncharacterized, the mechanistic summary indicates potential roles in cytoskeletal organization or intracellular trafficking. Coiled-coil proteins often participate in diverse complexes, such as those governing vesicle transport or ciliogenesis, hinting that CCDC149 disruption could impact these fundamental processes in HeLa cells.

In the HeLa cervical adenocarcinoma context, where HPV-mediated transformation disrupts key regulatory pathways, CCDC149’s contribution to cellular architecture and dynamics may be particularly revealing. Although upstream regulators and downstream effectors are undetermined, this knockout model enables systematic interrogation of CCDC149??s influence on processes like cell proliferation, migration, and invasion??phenotypes critical to cancer progression. The lack of functional annotation underscores the value of this tool for de novo discovery.

Researchers can employ this CCDC149 knockout polyclonal population in a range of assays to elucidate gene function. Knockout validation through western blotting and RT-qPCR confirms disruption, while immunofluorescence microscopy can visualize its impact on cellular structures. Functional studies might include cell proliferation, migration, and invasion assays to assess oncogenic contributions, and co-immunoprecipitation plus mass spectrometry to identify interacting partners. Global transcriptomic changes can be profiled via RNA-seq, offering insights into CCDC149??s role. For detailed product inquiries or technical support, please contact Ascent Research.

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