RGMa Double Nickase Plasmid (m): sc-434035-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RGMa 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
- RGMa Double Nickase Plasmid (m) and RGMa Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Rgma. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RGMa Double Nickase Plasmid (m) | sc-434035-NIC | 20 µg | $410.00 | |||
RGMa Double Nickase Plasmid (m2) | sc-434035-NIC-2 | 20 µg | $410.00 |
Mouse Rgma encodes repulsive guidance molecule A (RGMa), a glycosylphosphatidylinositol-anchored membrane protein that functions as an axon guidance cue and modulator of neuronal growth cone dynamics. RGMa engages receptors such as neogenin and influences downstream signaling that intersects with cytoskeletal remodeling, neurite outgrowth inhibition, and neuronal connectivity programs. It also participates in BMP pathway modulation and can shape cellular responses relevant to development, regeneration, and immune–neural interactions. Dysregulated RGMa signaling has been associated with neuroinflammatory and neurodegenerative contexts, making Rgma a useful target for mechanistic studies of circuit formation and injury responses in the mouse nervous system.
RGMa Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Rgma locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Rgma. 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 Rgma 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 Rgma-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.