The ART1 Knockout TE1 Polyclonal Cells product delivers a CRISPR/Cas9-edited polyclonal knockout cell population derived from TE1 human esophageal squamous cell carcinoma cells, designed to disrupt the ART1 gene. This polyclonal pool offers a heterogeneous loss-of-function model that avoids clonal selection artifacts, allowing researchers to investigate ART1 function in a genetically diverse background. The CRISPR/Cas9-mediated gene disruption ensures potent suppression of ART1 protein, enabling robust phenotypic and mechanistic studies.
The parental TE1 cell line is an widely utilized epithelial model of human esophageal squamous carcinoma, maintaining key features of the disease such as anchorage-independent growth and epithelial-to-mesenchymal plasticity. TE1 cells are extensively employed to dissect mechanisms of cancer cell adhesion, migration, invasion, and interactions with the tumor microenvironment, making them an ideal host for studying ART1??s role in esophageal cancer pathology.
ART1 encodes a mono-ADP-ribosyltransferase that attaches a single ADP-ribose moiety from NAD+ to arginine residues on target proteins, a reversible post-translational modification that regulates protein function. A prominent substrate of ART1 is integrin beta1, a transmembrane adhesion receptor that, upon ADP-ribosylation, exhibits altered signaling properties. This modification modulates the activation of focal adhesion kinase (FAK) and Src kinase, key transducers of integrin-mediated pathways governing cell adhesion, migration, and survival. Upstream, ART1 expression is stimulated by interferon-gamma (IFN-??), bacterial lipopolysaccharide (LPS), and pro-inflammatory cytokines, positioning ART1 at the nexus of immune signaling and integrin biology. The ART1-NAD+-integrin beta1-FAK/Src axis illustrates a critical signaling node linking extracellular inflammatory cues to cellular responses.
In the context of TE1 esophageal squamous carcinoma cells, ART1-dependent ADP-ribosylation of integrin beta1 and associated adhesion molecules is thought to enhance tumor cell motility, invasion, and resistance to anoikis, thereby promoting metastatic dissemination. By eliminating ART1 activity, this knockout model disrupts the arginine ADP-ribosylation-dependent regulation of integrin signaling, furnishing a powerful tool to dissect how this specific modification contributes to esophageal cancer aggressiveness. This system also facilitates exploration of ART1??s involvement in tumor microenvironment crosstalk and immune modulation, which are relevant to inflammatory and autoimmune conditions.
Researchers can employ this model in a variety of experiments, including western blotting for ART1 and downstream signaling effectors, in vitro ADP-ribosylation assays to quantify enzyme activity, cell adhesion and transwell migration/invasion assays, and flow cytometric analysis of integrin surface levels. Phospho-specific detection of FAK and Src provides direct readouts of integrin signaling status. The polyclonal population is suitable for transcriptome-wide studies via RNA-seq and for drug response profiling to uncover synthetic lethalities or resistance mechanisms. For additional information or to place an order, please contact Ascent Research.
