ARH1 Double Nickase Plasmid (m): sc-419017-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ARH1 Double Nickase Plasmid (m) 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
- ARH1 Double Nickase Plasmid (m) and ARH1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Adprh. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARH1 Double Nickase Plasmid (m) | sc-419017-NIC | 20 µg | $410.00 |
Mouse Adprh encodes ARH1, an ADP-ribosyl-acceptor hydrolase that reverses mono-ADP-ribosylation on arginine residues, thereby regulating the turnover of ADP-ribose marks on proteins. By controlling this post-translational modification, ARH1 contributes to NAD⁺-dependent signaling and broader ADP-ribosylation dynamics that intersect with cellular stress responses, metabolism, and protein function. Perturbation of arginine-linked ADP-ribosylation has been associated with dysregulated signaling networks and altered cellular homeostasis, making Adprh a useful locus for mechanistic studies of ADP-ribose biology. In mouse models, manipulating ARH1 activity helps interrogate how reversible ADP-ribosylation shapes tissue physiology and disease-relevant phenotypes without implying therapeutic outcomes.
ARH1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Adprh locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Adprh. 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 Adprh 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 Adprh-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.