PHLPPL Double Nickase Plasmid (m): sc-434083-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PHLPPL 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
- PHLPPL Double Nickase Plasmid (m) and PHLPPL Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Phlpp2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PHLPPL Double Nickase Plasmid (m) | sc-434083-NIC | 20 µg | $410.00 |
Phlpp2 encodes PHLPPL, a Ser/Thr protein phosphatase that dephosphorylates key signaling nodes including AKT, thereby tuning PI3K–AKT pathway amplitude, cell survival, and metabolic homeostasis in mouse cells. By counterbalancing kinase-driven phosphorylation, PHLPPL influences proliferation, stress responses, and insulin-related signaling outputs, and can shape downstream mTOR and FOXO-regulated transcriptional programs. Altered PHLPP family activity is associated with dysregulated growth and metabolic phenotypes in experimental models, making Phlpp2 a useful target for studying pathway rewiring under oncogenic or metabolic stress contexts.
PHLPPL Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Phlpp2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Phlpp2. 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 Phlpp2 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 Phlpp2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.