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Cat. No. ARG42970

CCDC167 Knockout AGS Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Adenocarcinoma

This CRISPR/Cas9-edited polyclonal knockout cell population disrupts CCDC167 in the AGS human gastric adenocarcinoma cell line, creating a loss-of-function model for studying the gene??s role in gastric cancer. CCDC167 encodes a coiled-coil domain-containing protein with unknown function, but its structural features suggest involvement in protein?Cprotein interactions, potentially impacting cancer cell phenotypes. Key applications include functional characterization, protein interaction screening, and biomarker discovery, employing techniques such as western blotting, proliferation and migration assays, co-immunoprecipitation, and RNA-seq transcriptomics. This model is suited for dissection of CCDC167-dependent signaling pathways and drug response in gastric adenocarcinoma.

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Shipping Info:

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

    CCDC167

    Gene Identifier

    NCBI Gene ID 154467

    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 CCDC167 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line, engineered for targeted disruption of the CCDC167 gene. As a polyclonal pool, this population maintains genetic heterogeneity across the genome while carrying CRISPR-induced loss-of-function mutations at the target locus, enabling robust functional studies without the clonal selection artifacts that can confound single-cell?Cderived knockout lines.

The AGS parental cell line was established from a primary gastric adenocarcinoma of a 54-year-old female and exhibits adherent epithelial morphology. These cells are microsatellite stable (MSS) and harbor wild-type TP53, representing a common genotype in gastric cancer. AGS cells are widely employed as an in vitro model for gastric adenocarcinoma, facilitating investigation of gastric cancer cell biology, intracellular signaling, and pharmacological responses.

CCDC167 encodes a putative coiled-coil domain-containing protein, a structural motif recurring in proteins that mediate homo- and heterotypic interactions. Although its precise biological function and interaction partners remain uncharacterized, CCDC167 is hypothesized to participate in the assembly or regulation of macromolecular complexes that may influence gastric cancer cell phenotypes. Currently, no defined upstream regulators, downstream effectors, or interacting factors have been identified for CCDC167. The provided mechanistic summary indicates that knockout of CCDC167 in AGS polyclonal cells leads to ablation of CCDC167 protein function, with anticipated consequences on protein interaction networks that could alter gastric cancer cell behavior.

Given the uncharacterized nature of CCDC167, this polyclonal knockout model provides a valuable tool for deorphanizing the gene and dissecting its contribution to gastric adenocarcinoma biology. In the context of the AGS cell line??a widely used platform for gastric cancer signaling and drug response studies??loss of CCDC167 may reveal novel phenotypes related to proliferation, migration, or survival, thereby shedding light on its potential involvement in tumorigenic processes.

Key research applications include functional characterization via proliferation, migration, and colony formation assays; protein interaction screening using co-immunoprecipitation and mass spectrometry; transcriptomic profiling by RNA-seq to identify CCDC167-dependent gene expression changes; and cell cycle analysis by flow cytometry. Knockout validation can be performed by western blotting and, where antibodies are available, immunostaining. These cells are also suitable for biomarker discovery and pairwise comparison with parental AGS cells in drug sensitivity screens. For further technical details, please contact Ascent Research.

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