ERMAP Double Nickase Plasmid (m): sc-424173-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ERMAP 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
- ERMAP Double Nickase Plasmid (m) and ERMAP Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ermap. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ERMAP Antibody (YS-6): sc-81790
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ERMAP Double Nickase Plasmid (m) | sc-424173-NIC | 20 µg | $410.00 |
Ermap encodes erythroblast membrane-associated protein (ERMAP), an immunoglobulin superfamily membrane glycoprotein enriched on erythroid lineage cells. In mouse, ERMAP contributes to erythrocyte membrane organization and participates in cell–cell recognition processes through its extracellular Ig-like domains, supporting erythroid maturation and red blood cell homeostasis. ERMAP is linked to blood group antigen biology and is used as a marker to study erythropoiesis, membrane stability, and immune-mediated interactions in hematopoietic tissues. Dysregulation of erythroid membrane proteins, including ERMAP-associated complexes, is relevant to models of anemia and altered red cell adhesion or clearance.
ERMAP Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ermap locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ermap. 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 Ermap 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 Ermap-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.