Perilipin Double Nickase Plasmid (m): sc-430499-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Perilipin 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
- Perilipin Double Nickase Plasmid (m) and Perilipin Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Plin1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Perilipin Double Nickase Plasmid (m) | sc-430499-NIC | 20 µg | $410.00 | |||
Perilipin Double Nickase Plasmid (m2) | sc-430499-NIC-2 | 20 µg | $410.00 |
Mouse Plin1 encodes perilipin, a lipid droplet–associated scaffold that regulates adipocyte triglyceride storage by controlling access of cytosolic lipases to the droplet surface. Perilipin integrates PKA-driven phosphorylation signals to coordinate ATGL and hormone-sensitive lipase activity during lipolysis, thereby coupling cAMP signaling to fatty acid mobilization and energy homeostasis. Altered Plin1 expression or function perturbs lipid droplet dynamics and adipose tissue metabolism, making it relevant to studies of obesity, insulin resistance, hepatic steatosis, and inflammation linked to dysregulated lipid handling. In addition to adipocytes, Plin1-dependent lipid droplet remodeling is used to probe organellar crosstalk, including ER–lipid droplet interactions and oxidative stress responses.
Perilipin Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Plin1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Plin1. 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 Plin1 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 Plin1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.