Peg1 Double Nickase Plasmid (m): sc-421634-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Peg1 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
- Peg1 Double Nickase Plasmid (m) and Peg1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Mest. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Peg1 Double Nickase Plasmid (m) | sc-421634-NIC | 20 µg | $410.00 |
Mouse Mest, also known as Peg1, is an imprinted gene encoding a membrane-associated protein implicated in embryonic and placental development, adipocyte differentiation, and growth regulation. Peg1/MEST activity has been linked to epigenetic control mechanisms, including parent-of-origin–specific expression and DNA methylation at imprinting control regions, which influence transcriptional programs during development. Altered Mესტ/MEST expression or imprinting status is associated with abnormal fetal growth, placental insufficiency, and metabolic phenotypes such as changes in adiposity. In cancer biology, dysregulated MEST has been reported as a feature of tumor-associated epigenetic reprogramming, making it relevant for studies of imprinting, developmental pathways, and cell state transitions.
Peg1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Mest locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Mest. 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 Mest 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 Mest-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.