ART1 Knockout KYSE-150 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human esophageal squamous cell carcinoma cell line KYSE-150. This product provides a genetically disrupted ART1 gene locus using a non-clonal, pooled format, enabling researchers to investigate the loss-of-function effects on ADP-ribosylation-dependent processes in a cancer-relevant background.
The KYSE-150 cell line is a widely used model of esophageal squamous cell carcinoma, exhibiting characteristics of cancerous epithelial cells. Originating from a well-differentiated esophageal squamous cell carcinoma, these cells retain key signaling networks relevant to tumor biology, including those governing cell adhesion, migration, and proliferation.
ART1 encodes an arginine-specific mono-ADP-ribosyltransferase that post-translationally modifies target proteins such as integrin ??1. This modification regulates cell adhesion and activates downstream signaling cascades involving focal adhesion kinase (FAK), phosphoinositide 3-kinase (PI3K), and AKT. ART1 expression is known to be regulated by upstream factors including interferon-gamma (IFN-??), tumor necrosis factor-alpha (TNF-??), and NF-??B. Through its enzymatic activity, ART1 influences cell adhesion, migration, proliferation, and apoptosis, making it a pivotal modulator of oncogenic signaling.
In the context of esophageal squamous cell carcinoma, ART1-mediated ADP-ribosylation of integrin ??1 has been implicated in promoting cell proliferation and migration. Disruption of ART1 in KYSE-150 polyclonal cells is expected to attenuate these oncogenic processes, providing a physiologically relevant model to dissect ART1’s contribution to cancer progression. This knockout population allows for the study of both cell-autonomous effects and the broader impact on integrin signaling within an epithelial tumor environment.
Typical research applications include investigating the role of ADP-ribosylation in esophageal cancer biology, assessing ART1-dependent regulation of cell adhesion and migration, screening for small-molecule inhibitors of ART1, and evaluating the impact of ART1 loss on downstream signaling pathways. This product is compatible with assays such as western blotting for ADP-ribosylation and signaling proteins, migration and invasion assays, proliferation assays, cell adhesion assays, and flow cytometry for integrin expression. For further technical details and support, please contact Ascent Research.
