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Cat. No. ARG42610

CAV1 Knockout AGS Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Adenocarcinoma

CAV1 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from AGS gastric adenocarcinoma cells, providing a heterogeneous loss-of-function model for caveolin-1. The CAV1 gene encodes a scaffolding protein that regulates endocytosis, cholesterol homeostasis, and signal transduction by interacting with key molecules such as EGFR and Akt. These polyclonal knockout cells enable robust investigation of caveolae dysfunction, integrin signaling, and oncogenic pathways in gastric cancer. Applications include Western blotting, proliferation assays, and drug sensitivity studies, making them ideal for dissecting caveolin-1's role in tumor suppression and Helicobacter pylori pathogenesis. For further information, contact Ascent Research.

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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

    CAV1

    Gene Identifier

    NCBI Gene ID 857

    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

CAV1 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from AGS gastric adenocarcinoma cells. The product provides a heterogeneous pool of cells with targeted disruption of the CAV1 gene, enabling loss-of-function studies without clonal selection bias. This polyclonal format preserves genetic diversity while ensuring robust CAV1 deficiency across the population, ideal for high-throughput screening and functional assays.

The AGS cell line originates from a human gastric adenocarcinoma, serving as a well-characterized epithelial model for studying gastric cancer biology. AGS cells exhibit adherent morphology and retain key signaling properties of gastric epithelial cells, including responsiveness to growth factors and microbial challenges such as Helicobacter pylori infection. Their widespread use in cancer research makes them a suitable host for investigating tumorigenic mechanisms.

CAV1 encodes caveolin-1, a scaffolding protein essential for caveolae formation. Caveolin-1 regulates endocytosis, cholesterol homeostasis, and signal transduction by interacting with numerous signaling molecules. Upstream, CAV1 expression is regulated by TGF-??, cholesterol, PPAR??, FOXO transcription factors, and SREBP. Downstream, caveolin-1 interacts with and modulates the activity of eNOS, Src kinases, H-Ras, EGFR, ??-catenin, and Akt. It forms complexes with cavin family proteins, integrins, and TGF-?? receptors, integrating pathways such as caveolae-mediated endocytosis, integrin signaling, MAPK/ERK, PI3K/Akt, TGF-?? signaling, and Wnt/??-catenin signaling.

In AGS gastric adenocarcinoma cells, CAV1 knockout disrupts caveolae formation, altering integrin-mediated adhesion and signaling. Loss of caveolin-1 may relieve its tumor-suppressive interactions with growth factor receptors, potentially leading to enhanced proliferation through constitutive activation of MAPK and Akt pathways. This model is particularly relevant for dissecting the dual role of caveolin-1 in gastric cancer, where it can act as a context-dependent tumor suppressor or promoter, and for examining its contribution to processes such as epithelial-mesenchymal transition, drug resistance, and Helicobacter pylori pathogenesis.

CAV1 Knockout AGS Polyclonal Cells are a versatile tool for gastric cancer research, enabling investigations into caveolae dysfunction, endocytosis, and oncogenic signaling. Typical applications include Western blotting for CAV1 expression, immunofluorescence for caveolae assessment, cell proliferation (MTT) and invasion/migration assays, RT-qPCR for downstream targets, phospho-ERK/Akt analysis, cholesterol modulation experiments, and co-immunoprecipitation for protein interactions. These cells also support drug sensitivity profiling and H. pylori infection studies. For further information, please contact Ascent Research.

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