MS4A7 Double Nickase Plasmid (m): sc-430914-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MS4A7 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
- MS4A7 Double Nickase Plasmid (m) and MS4A7 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ms4a7. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MS4A7 Double Nickase Plasmid (m) | sc-430914-NIC | 20 µg | $410.00 |
Ms4a7 encodes MS4A7, a tetraspan membrane protein enriched in monocytes and macrophages and frequently used as a marker of myeloid differentiation. MS4A7 is implicated in plasma membrane microdomain organization and regulation of immune receptor signaling, influencing processes such as phagocytosis, migration, and inflammatory activation. In mouse tissues and tumor microenvironments, Ms4a7 expression correlates with macrophage infiltration and functional polarization, linking it to innate immune networks including cytokine and chemokine signaling. Altered myeloid states marked by MS4A7 have been associated with inflammatory pathology and cancer-associated macrophage biology, making Ms4a7 a useful node for dissecting immune cell programs.
MS4A7 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ms4a7 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ms4a7. 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 Ms4a7 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 Ms4a7-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.