PMM2 Double Nickase Plasmid (m): sc-424790-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PMM2 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
- PMM2 Double Nickase Plasmid (m) and PMM2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Pmm2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PMM2 Double Nickase Plasmid (m) | sc-424790-NIC | 20 µg | $410.00 | |||
PMM2 Double Nickase Plasmid (m2) | sc-424790-NIC-2 | 20 µg | $410.00 |
Mouse Pmm2 encodes phosphomannomutase 2 (PMM2), a cytosolic enzyme that interconverts mannose-6-phosphate and mannose-1-phosphate to support GDP-mannose and dolichol-linked oligosaccharide biosynthesis. This activity links Pmm2 to N-glycosylation and broader glycan assembly processes that influence protein folding, trafficking, and extracellular matrix interactions. Perturbation of PMM2 function disrupts proteostasis and cell-surface glycosylation patterns, impacting secretory pathway homeostasis and intercellular signaling. Pmm2 is therefore widely studied in models of congenital disorders of glycosylation and in systems-level analyses of glycan-dependent regulation of development, immunity, and metabolism.
PMM2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Pmm2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Pmm2. 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 Pmm2 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 Pmm2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.