LRP16 Double Nickase Plasmid (m): sc-430699-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LRP16 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
- LRP16 Double Nickase Plasmid (m) and LRP16 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Macrod1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LRP16 Double Nickase Plasmid (m) | sc-430699-NIC | 20 µg | $410.00 |
Macrod1 encodes LRP16, a nuclear macrodomain-containing protein that binds mono-ADP-ribose and interfaces with PARP-dependent ADP-ribosylation signaling. In mouse cells, LRP16 has been linked to regulation of chromatin-associated processes including transcriptional control, DNA damage responses, and cell-cycle–coupled genome maintenance. Through these functions, MACROD1/LRP16 is studied in pathways connecting nuclear receptor signaling, stress responses, and post-translational modification dynamics. Altered expression or dysregulated activity of LRP16 is frequently investigated in contexts of proliferation control and genomic instability relevant to cancer biology and inflammatory signaling models.
LRP16 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Macrod1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Macrod1. 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 Macrod1 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 Macrod1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.