The ART1 Knockout MCF-7 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population targeting the ART1 gene (ADP-ribosyltransferase 1) in the MCF-7 human breast adenocarcinoma cell line. This loss-of-function model is generated via CRISPR/Cas9-mediated gene disruption, yielding a heterogeneous pool of cells with abrogated ART1 expression. As polyclonal knockout cells, they avoid artifacts of monoclonal selection and provide a more representative system for studying gene function. This product is designed for researchers investigating protein mono-ADP-ribosylation, integrin signaling, and tumor progression.
MCF-7 is a widely utilized epithelial cell line established from the pleural effusion of metastatic breast adenocarcinoma. These cells are estrogen receptor-positive, progesterone receptor-positive, and hormone-responsive, serving as a principal model for luminal A subtype breast cancer. MCF-7 cells are extensively employed in investigations of hormone signaling, metastasis, and drug sensitivity. Their well-characterized biology and standardized culture conditions make them an ideal host for genetic manipulation and functional studies of cancer-related genes.
ART1 catalyzes the mono-ADP-ribosylation of arginine residues on target proteins such as integrin alpha7, integrin beta1, and the P2X7 purinergic receptor, thereby modulating protein function. Its activity is upregulated by pro-inflammatory cytokines (TNF-alpha, IFN-gamma) and growth factors (TGF-beta1). ART1 functions within focal adhesion and integrin signaling pathways, interacting with effectors like FAK (PTK2), Src, paxillin, talin, vinculin, ILK, Akt, and ERK. Through these interactions, ART1 influences cell adhesion, migration, and ECM-receptor crosstalk, while also intersecting with NAD+ metabolism. The enzyme’s role in modifying cell surface proteins positions it as a key regulator of adhesion dynamics and immune-related signaling.
In MCF-7 cells, knockout of ART1 is predicted to disrupt integrin-mediated adhesion and downstream signaling, potentially attenuating migratory and invasive properties associated with metastatic progression. The loss of ART1-dependent ADP-ribosylation may alter cellular responsiveness to cytokines and extracellular matrix cues. This model enables dissection of ART1-specific functions independent of closely related ADP-ribosyltransferases such as ART3 and ART4, and facilitates study of NAD+ homeostasis in breast cancer contexts. The polyclonal nature preserves native genetic variation, offering a more physiologically relevant experimental system.
This knockout model supports a diverse range of applications, including cell adhesion assays, Transwell migration/invasion studies, western blotting and RT-qPCR for ART1 and downstream targets, flow cytometry for integrin expression, and immunofluorescence for focal adhesion visualization. Researchers can also perform phospho-signaling analysis of FAK and Src activation, NAD+ level measurement, co-immunoprecipitation of ART1 substrates, and MTT proliferation assays. These tools are valuable for probing the role of ART1 in drug response, tumor microenvironment interactions, and breast cancer metastasis. For additional technical support, please contact Ascent Research.
