The ART1 Knockout Ca Ski Polyclonal Cells product provides a mixed population of Ca Ski human cervical carcinoma cells in which the ART1 gene has been disrupted using CRISPR/Cas9 genome editing. As a polyclonal knockout pool, this model offers a heterogeneous loss-of-function system suitable for studying the cellular functions of ART1 without the limitations of single-cell clonal selection. This product is designed for researchers investigating mono-ADP-ribosylation signaling in an oncogenic HPV-16 positive epithelial background.
Ca Ski cells are an adherent epithelial cell line originally derived from an epidermoid carcinoma of the uterine cervix. These cells are persistently infected with human papillomavirus type 16 (HPV-16), making them a well-established model for studying cervical cancer biology, viral oncogenesis, and epithelial cell transformation. The integration of HPV-16 oncogenes E6 and E7 contributes to their transformed phenotype, providing a relevant context for evaluating host factors involved in tumor progression.
The ART1 gene encodes an arginine-specific mono-ADP-ribosyltransferase that catalyzes the covalent transfer of ADP-ribose from NAD? to arginine residues on target proteins. Among its substrates are integrins (??7??1, ??L??2, ??4??1), the P2X7 purinergic receptor, and heparin-binding EGF-like growth factor (HB-EGF). ART1 is transcriptionally upregulated by pro-inflammatory stimuli including IFN-??, TNF-??, and IL-1??, acting through STAT1 and NF-??B. Through modification of cell surface proteins, ART1 modulates integrin-mediated cell adhesion and migration, as well as downstream signaling cascades such as FAK/Src, Rho GTPases, NF-??B, and MAPK1/3 (ERK1/2). ART1 also interacts with ARTC2, another ADP-ribosyltransferase, and its activity influences both cell-extracellular matrix and cell-cell interactions.
In the Ca Ski cervical carcinoma background, knockout of ART1 is expected to alter the adhesive and migratory properties driven by HPV-16 oncoproteins. Given ART1??s role in regulating integrin function, its loss may disrupt focal adhesion dynamics and impair signaling through focal adhesion kinase (FAK) and Src, thereby affecting tumor cell motility and invasiveness. Furthermore, ART1-dependent ADP-ribosylation of HB-EGF could modulate growth factor signaling, while modification of the P2X7 receptor may influence inflammatory responses. This polyclonal knockout model thus provides a valuable tool to dissect the contribution of ADP-ribosylation to HPV-driven malignancy, particularly in the context of immune evasion and metastatic potential.
Typical research applications include investigating the role of ART1 in cervical cancer progression, studying the functional consequences of integrin ADP-ribosylation on cell adhesion and migration, and examining crosstalk with HPV oncoprotein pathways. The product is well-suited for assays such as Western blotting and RT-qPCR for confirmation of ART1 disruption, immunofluorescence microscopy for localization, cell adhesion assays on fibronectin or collagen substrates, Boyden chamber migration and invasion assays, flow cytometry for integrin surface expression, ADP-ribosylation activity assays, and phospho-FAK immunoblotting. Additionally, it can be applied in drug target validation and inflammatory response modulation studies. For further technical details or ordering information, please contact Ascent Research.
