Per2 Double Nickase Plasmid (m): sc-422193-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Per2 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
- Per2 Double Nickase Plasmid (m) and Per2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Per2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Per2 Double Nickase Plasmid (m) | sc-422193-NIC | 20 µg | $410.00 |
Mouse Per2 (Period circadian regulator 2) encodes a core component of the molecular circadian clock that participates in the transcriptional–translational feedback loop controlling rhythmic gene expression. PER2 forms complexes with other clock proteins to modulate CLOCK–BMAL1 activity, shaping oscillations in metabolism, cell cycle progression, DNA damage responses, and neuronal and endocrine signaling. Altered Per2 function has been associated with disrupted circadian rhythms and downstream changes in inflammatory signaling, metabolic homeostasis, and stress-response pathways. In biomedical research, Per2 is frequently studied for its role in timing-dependent regulation of physiology and for how circadian dysregulation influences disease-relevant phenotypes in mouse models.
Per2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Per2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Per2. 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 Per2 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 Per2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.