METRNL Double Nickase Plasmid (m): sc-431669-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- METRNL 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
- METRNL Double Nickase Plasmid (m) and METRNL Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Metrnl. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
METRNL Double Nickase Plasmid (m) | sc-431669-NIC | 20 µg | $410.00 | |||
METRNL Double Nickase Plasmid (m2) | sc-431669-NIC-2 | 20 µg | $410.00 |
Metrnl encodes meteorin-like (METRNL), a secreted, glycosylated protein implicated in intercellular signaling that coordinates metabolic and inflammatory programs. In mouse tissues, METRNL expression has been linked to adipose–immune crosstalk, modulation of macrophage polarization, and regulation of energy homeostasis in response to physiological stressors such as cold exposure and exercise. Reported functional connections include pathways influencing cytokine signaling and extracellular matrix remodeling, positioning METRNL as a useful node for studying systemic metabolism and tissue adaptation. Dysregulated METRNL-associated signaling has been investigated in contexts of obesity, insulin resistance, and inflammatory phenotypes, supporting mechanistic research into metabolic disease–relevant pathways.
METRNL Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Metrnl locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Metrnl. 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 Metrnl 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 Metrnl-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.