ART1 Knockout T-47D Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population derived from the T-47D human breast epithelial adenocarcinoma line, with targeted disruption of the ART1 gene. This polyclonal knockout model provides a heterogeneous loss-of-function system for studying mono-ADP-ribosyltransferase activity without the clonal biases inherent to monoclonal lines, facilitating robust functional analyses.
The T-47D host line was established from the pleural effusion of a 54-year-old female with invasive ductal carcinoma. It is characterized by positive expression of estrogen receptor (ER), progesterone receptor (PR), and androgen receptor (AR), with no HER2 amplification, representing a well-established luminal A breast cancer model. T-47D cells retain epithelial morphology and hormone responsiveness, making them particularly suitable for investigating adhesion-dependent signaling and metastatic progression.
ART1 encodes a glycosylphosphatidylinositol (GPI)-anchored mono-ADP-ribosyltransferase that catalyzes the transfer of ADP-ribose from NAD+ to arginine residues on target proteins, notably integrin ??7. This post-translational modification governs integrin ??7??1 binding to fibronectin and the actin cytoskeleton, thereby regulating cell adhesion, migration, and apoptosis. Significantly, ART1 is activated by IL-6/STAT3, TNF-??, and EGF pathways, and its downstream effects involve focal adhesion kinase (FAK), Src, RhoA, and caspases. ART1 resides in lipid raft microdomains, where it interacts with integrins and other signaling components to modulate extracellular matrix sensing and immune evasion.
In the T-47D breast cancer context, disruption of ART1 compromises integrin ADP-ribosylation, potentially impairing cell adhesion, migration, and anoikis resistance. This knockout model enables dissection of how mono-ADP-ribosylation intersects with endocrine signaling and inflammatory cues (e.g., IL-6, TNF-??) that drive tumor progression and immune escape.
These polyclonal knockout cells support a range of research applications, including cancer cell adhesion studies, breast cancer metastasis mechanistic investigations, and validation of mono-ADP-ribosylation targets. Assays such as Western blotting, RT-qPCR, cell adhesion and transwell migration/invasion tests, annexin V apoptosis analysis, NAD+ consumption measurements, and ADP-ribosylation mass spectrometry are readily applicable. In vivo, these cells facilitate xenograft tumor models to evaluate metastatic potential and immune modulation. For additional information or technical support, please contact Ascent Research.
