MR1 Double Nickase Plasmid (m): sc-420785-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MR1 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
- MR1 Double Nickase Plasmid (m) and MR1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Mr1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MR1 Double Nickase Plasmid (m) | sc-420785-NIC | 20 µg | $410.00 | |||
MR1 Double Nickase Plasmid (m2) | sc-420785-NIC-2 | 20 µg | $410.00 |
Mouse MR1 (MHC class I-related protein 1) is a non-classical antigen-presenting molecule that binds small metabolite-derived ligands and displays them at the cell surface for recognition by mucosal-associated invariant T (MAIT) cells. Through this MR1–MAIT axis, MR1 contributes to immune surveillance and rapid cytokine responses at barrier tissues, linking cellular metabolic state to innate-like T cell activation. MR1-dependent signaling influences inflammatory programs and host responses to microbial metabolites, making it relevant to studies of infection, mucosal immunity, and immune regulation in inflammatory disease models. Altered MR1 presentation and MAIT cell activity are also investigated in settings of tumor immunology and metabolic inflammation to understand how ligand availability shapes immune function.
MR1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Mr1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Mr1. 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 Mr1 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 Mr1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.