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Cat. No. ARG43051

CCDC71L Knockout AGS Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Adenocarcinoma

The CCDC71L Knockout AGS Polyclonal Cells are a polyclonal knockout population generated by CRISPR/Cas9-mediated disruption of the CCDC71L gene in AGS human gastric adenocarcinoma cells. These cells offer a loss-of-function model for studying the poorly characterized coiled-coil domain protein CCDC71L, which may play roles in protein-protein interactions, cytoskeletal organization, or signaling pathways relevant to gastric cancer. Researchers can employ these cells to investigate CCDC71L's function in gastric epithelial biology, including proliferation, migration, and invasion assays, as well as protein interaction studies and transcriptomic profiling. This model supports functional genomics screens for tumor suppressors or oncogenes in gastric adenocarcinoma.

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Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    AGS

    Sex of Donor

    Female

    Age

    54 years

    Derived From Site

    In situ; Stomach

    Gene Name

    CCDC71L

    Gene Identifier

    NCBI Gene ID 168455

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    Ham's F-12

    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 CCDC71L Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line. These cells feature targeted disruption of the CCDC71L gene, encoding a coiled-coil domain protein of unknown function. This heterogeneous loss-of-function model enables study of CCDC71L-dependent phenotypes in a gastric epithelial context, providing a tool for functional genomics research.

The AGS cell line (ATCC CRL-1739) originates from a poorly differentiated gastric adenocarcinoma in a 54-year-old woman. AGS cells display adherent epithelial morphology and serve as a model for gastric epithelial biology, H. pylori infection, and cancer signaling studies, making them suitable for investigating genes relevant to gastric adenocarcinoma.

CCDC71L contains coiled-coil domains that mediate protein-protein interactions, but its biological function is largely uncharacterized. Coiled-coil domains are involved in cytoskeletal organization and signaling complex assembly, suggesting CCDC71L may participate in these processes. Its knockout could disrupt protein interaction networks, potentially affecting cytoskeletal dynamics or signaling pathways such as Wnt signaling in gastric epithelial cells. The loss-of-function model thus offers a means to explore CCDC71L’s role in cellular architecture and signal transduction.

Knocking out CCDC71L in AGS cells provides a relevant platform to investigate its potential contributions to gastric adenocarcinoma phenotypes, including proliferation, migration, and invasion. The AGS background enables studies of host-pathogen interactions with H. pylori, a gastric cancer risk factor. The polyclonal nature avoids clonal biases, yielding a more representative assessment of CCDC71L’s functional impact.

The cells are suitable for Western blotting and RT-qPCR to confirm CCDC71L loss, and proliferation, migration, and invasion assays to assess phenotypic changes. Co-immunoprecipitation can identify protein interaction partners, while RNA-seq permits transcriptome-wide analysis. These tools support functional genomics screening for gastric cancer-related genes. For further details, contact Ascent Research.

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