ARH1 Double Nickase Plasmid (h): sc-410678-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ARH1 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
- ARH1 Double Nickase Plasmid (h) and ARH1 Double Nickase Plasmid (h2) 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 (h) | sc-410678-NIC | 20 µg | $410.00 | |||
ARH1 Double Nickase Plasmid (h2) | sc-410678-NIC-2 | 20 µg | $410.00 |
Human ADPRH encodes ADP-ribosylarginine hydrolase 1 (ARH1), a cytosolic enzyme that removes ADP-ribose from arginine residues to reverse mono-ADP-ribosylation. By restoring native protein side chains after ADP-ribosyltransferase activity, ARH1 contributes to regulation of post-translational modification dynamics that influence signaling, cytoskeletal remodeling, and stress responses. This de-ADP-ribosylation activity interfaces with broader ADP-ribose biology relevant to host–pathogen interactions and cellular homeostasis. Dysregulated ADP-ribosylation turnover has been associated with altered inflammatory signaling and genome maintenance pathways, making ADPRH a useful locus for mechanistic studies of pathway control.
ARH1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ADPRH locus in human 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.