Apelin Double Nickase Plasmid (m): sc-424407-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Apelin 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
- Apelin Double Nickase Plasmid (m) and Apelin Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Apln. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Apelin Double Nickase Plasmid (m) | sc-424407-NIC | 20 µg | $410.00 |
Mouse Apln encodes apelin, a secreted peptide ligand for the APJ/APLNR G protein–coupled receptor that regulates cardiovascular homeostasis, angiogenesis, fluid balance, and metabolic signaling. Apelin–APJ engagement activates PI3K–AKT, ERK/MAPK, and AMPK-linked pathways to influence endothelial cell migration, nitric oxide production, and vascular remodeling, and it intersects with hypoxia-driven programs such as HIF-dependent responses. In the central nervous system and peripheral tissues, apelin contributes to neuroendocrine regulation and energy balance, with context-dependent effects on inflammation and fibrosis-associated processes. Altered Apln/apelin signaling is frequently studied in models of heart failure, hypertension, ischemia, metabolic dysfunction, and tumor-associated angiogenesis to understand pathway-level drivers of disease phenotypes.
Apelin Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Apln locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Apln. 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 Apln 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 Apln-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.