OLFM2 Double Nickase Plasmid (m): sc-434096-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- OLFM2 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
- OLFM2 Double Nickase Plasmid (m) and OLFM2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Olfm2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
OLFM2 Double Nickase Plasmid (m) | sc-434096-NIC | 20 µg | $410.00 |
Olfm2 encodes olfactomedin 2 (OLFM2), a secreted/ECM-associated glycoprotein enriched in neural tissues that contributes to extracellular matrix organization and cell–cell communication. OLFM2 has been linked to neuronal differentiation, neurite outgrowth, and synapse-related processes through interactions with membrane and matrix components that influence adhesion and signaling. In mouse models and human association studies, altered OLFM2 activity has been connected to neurodevelopmental and neurodegenerative phenotypes, including pathways relevant to retinal ganglion cell integrity and stress responses. These features make Olfm2 a useful target for dissecting ECM-mediated regulation of neural circuitry and vulnerability in disease-relevant contexts.
OLFM2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Olfm2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Olfm2. 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 Olfm2 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 Olfm2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.