ARH2 Double Nickase Plasmid (m): sc-433335-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ARH2 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
- ARH2 Double Nickase Plasmid (m) and ARH2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Adprhl1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARH2 Double Nickase Plasmid (m) | sc-433335-NIC | 20 µg | $410.00 | |||
ARH2 Double Nickase Plasmid (m2) | sc-433335-NIC-2 | 20 µg | $410.00 |
Mouse Adprhl1 encodes ARH2, an ADP-ribosylhydrolase-like protein implicated in the turnover or recognition of ADP-ribosylation signals that couple cellular metabolism to stress responses. ADP-ribosylation interfaces with DNA damage signaling, chromatin regulation, and transcriptional control, linking ARH2-associated processes to genome stability and cellular homeostasis. In experimental systems, perturbation of ADP-ribose signaling is frequently associated with altered cell survival, inflammatory signaling, and remodeling of cytoskeletal or mitochondrial functions, making Adprhl1 a useful node for pathway dissection. These connections provide disease-relevant context for studying how ADP-ribose–dependent regulation contributes to cardiometabolic and neurobiological phenotypes without implying clinical outcomes.
ARH2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Adprhl1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Adprhl1. 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 Adprhl1 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 Adprhl1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.