The ART1 Knockout HAP1 Polyclonal Cells product provides a heterogeneous pool of CRISPR/Cas9-edited HAP1 cells harboring disruptive mutations at the ART1 locus, generating a loss-of-function model for studying ADP-ribosylation-dependent immune regulation. This polyclonal population is derived from the near-haploid HAP1 cell line, enabling robust functional genomics applications without the confounding effects of diploid gene compensation. The knockout disrupts ART1-mediated post-translational modification, allowing researchers to dissect its role in immune cell adhesion and inflammatory signaling.
HAP1 cells are a near-haploid human cell line adapted to adherent growth from the KBM-7 chronic myeloid leukemia background. Their haploid karyotype simplifies genetic screens and knockout studies, as a single CRISPR targeting event can produce a null phenotype. This feature makes HAP1 an ideal host for generating polyclonal knockout populations, where a bulk-edited pool retains near-complete gene disruption, facilitating scalable, cost-effective loss-of-function experiments in a defined genetic context.
ART1 (ADP-ribosyltransferase 1) is a glycosylphosphatidylinositol (GPI)-anchored ectoenzyme that catalyzes mono-ADP-ribosylation of arginine residues on target proteins, utilizing NAD+ as a substrate. This modification modulates the function of key immune receptors and adhesion molecules. Upstream, ART1 expression is induced by proinflammatory cytokines such as interferon-gamma (IFNG), tumor necrosis factor (TNF), and interleukin-1 beta (IL-1B). Downstream, it modifies integrin alpha-7 (ITGA7), the purinergic receptor P2X7R, and other cell surface proteins, thereby influencing integrin-mediated adhesion and purinergic signaling. ART1 localizes to lipid rafts, positioning it to rapidly ADP-ribosylate proteins involved in immune cell trafficking and activation.
Disruption of ART1 in HAP1 cells provides a unique platform to investigate how ADP-ribosylation governs immune cell behavior in a simplified genetic background. The absence of functional ART1 allows direct assessment of the role of arginine-specific mono-ADP-ribosylation in modulating cell?Cmatrix and cell?Ccell interactions, inflammatory responses, and downstream signaling pathways. Given the involvement of ART1 in immune disorders, inflammatory diseases, and cancer, this knockout model supports mechanistic studies and drug target validation without interference from wild-type alleles.
Researchers can employ ART1 Knockout HAP1 Polyclonal Cells in a variety of experimental contexts, including ADP-ribosylation assays, cell adhesion assays, flow cytometry, western blotting, RT-qPCR, and immunofluorescence. Applications range from dissecting integrin-mediated adhesion dynamics to screening for modulators of ART1 activity in inflammatory pathways. The polyclonal nature of the knockout population ensures high editing efficiency while avoiding clonal artifacts, making it suitable for both acute loss-of-function experiments and long-term genetic studies. For further details or to order, please contact Ascent Research.
