ART1 Double Nickase Plasmid (h): sc-403742-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ART1 Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- ART1 Double Nickase Plasmid (h) and ART1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ART1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ART1 Double Nickase Plasmid (h) | sc-403742-NIC | 20 µg | $410.00 | |||
ART1 Double Nickase Plasmid (h2) | sc-403742-NIC-2 | 20 µg | $410.00 |
ART1 (ecto-ADP-ribosyltransferase 1) is a glycosylphosphatidylinositol-anchored, cell-surface enzyme that catalyzes mono-ADP-ribosylation of target proteins using extracellular NAD+. This post-translational modification can influence receptor signaling, cell–cell interactions, and adhesion dynamics, and has been linked to modulation of immune and inflammatory responses. ART1 activity is associated with regulation of purinergic signaling and extracellular NAD+-dependent pathways that shape cellular communication within tissue microenvironments. Altered ART1 expression or activity has been reported in contexts relevant to cancer biology, airway inflammation, and vascular cell function, supporting its use as a mechanistic node for studying extracellular ADP-ribosylation in human cells.
ART1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ART1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ART1. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt ART1 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of ART1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.