CD73 Double Nickase Plasmid (m): sc-423919-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CD73 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
- CD73 Double Nickase Plasmid (m) and CD73 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Nt5e. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD73 Double Nickase Plasmid (m) | sc-423919-NIC | 20 µg | $410.00 | |||
CD73 Double Nickase Plasmid (m2) | sc-423919-NIC-2 | 20 µg | $410.00 |
Mouse Nt5e encodes CD73 (ecto-5′-nucleotidase), a GPI-anchored ectoenzyme that catalyzes the dephosphorylation of extracellular AMP to adenosine, shaping purinergic signaling and nucleotide metabolism in the tissue microenvironment. By controlling local adenosine availability, CD73 influences cAMP-linked signaling, immune cell activation states, endothelial barrier biology, and hypoxia-associated responses. CD73 activity interfaces with the ATP–adenosine axis alongside CD39 and adenosine receptors to regulate inflammation, vascular remodeling, and metabolic adaptation. Dysregulated CD73 expression or activity is implicated in models of chronic inflammation, ischemic injury, fibrosis, and tumor-associated immune suppression, supporting its relevance in mechanistic studies.
CD73 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Nt5e locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Nt5e. 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 Nt5e 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 Nt5e-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.