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Home / Products / Genome-edited Cells / Knockout Cell Lines / KRT18 Knockout AGS Polyclonal Cells

Cat. No. ARG35303

KRT18 Knockout AGS Polyclonal Cells

Product Type:
Polyclonal Cell Population
Species:
Homo sapiens (Human)
Tissue Source:
Stomach
Disease:
Adenocarcinoma

Datasheet

The KRT18 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population from AGS gastric adenocarcinoma cells, enabling loss-of-function studies of keratin 18. KRT18 heterodimerizes with KRT8, is regulated by EGFR, Akt, and caspases, and modulates Bcl-xL and NF-??B signaling. Disruption of KRT18 impairs epithelial filament networks, altering apoptosis, adhesion, and migration in a p53-deficient background. This model is suited for gastric cancer progression, EMT, drug resistance, and biomarker discovery using Western blotting, immunofluorescence, and apoptosis assays.

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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

KRT18

Gene Identifier

NCBI Gene ID 3875

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 KRT18 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from AGS gastric adenocarcinoma cells, with disruption of the KRT18 gene. This heterogeneous pool enables robust loss-of-function studies without clonal selection, suitable for advanced cancer and epithelial biology research.

AGS cells originate from a 54-year-old female patient with gastric adenocarcinoma and are p53-deficient, providing a model for gastric epithelial carcinogenesis with impaired DNA damage responses. These cells maintain epithelial characteristics, making them relevant for studying keratin function in tumor progression.

KRT18 is a type I intermediate filament protein that forms obligate heterodimers with KRT8, establishing the epithelial intermediate filament network. It is phosphorylated by EGFR, PKC, and Akt, and cleaved by caspases during apoptosis. KRT18 interacts with desmoplakin, plakoglobin, 14-3-3 proteins, and TRADD, and regulates downstream effectors such as Bcl-xL and NF-??B. CRISPR-mediated KRT18 disruption destabilizes filament networks, attenuates caspase-mediated cleavage, and may promote anchorage-independent growth.

In p53-null AGS cells, KRT18 knockout compromises cell adhesion and polarity, potentially driving epithelial-mesenchymal transition and invasion. Combined with defective apoptosis, this model recapitulates key features of gastric cancer aggressiveness and resistance mechanisms, offering a platform to study cytoskeletal signaling crosstalk with EGFR/Akt and TNF-??/NF-??B pathways.

These polyclonal knockout cells support diverse assays: Western blotting and RT-qPCR for KRT18/KRT8 expression; immunofluorescence for filament integrity; flow cytometry (Annexin V) and caspase activity for apoptosis; migration/invasion and MTT assays for functional readouts; co-immunoprecipitation of KRT8/18 complexes; and phospho-EGFR/Akt analysis. Applications include gastric cancer progression, EMT, drug resistance, and biomarker discovery. For further information, contact Ascent Research.