PTP1B Double Nickase Plasmid (m): sc-422502-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PTP1B 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
- PTP1B Double Nickase Plasmid (m) and PTP1B Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ptpn1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PTP1B Double Nickase Plasmid (m) | sc-422502-NIC | 20 µg | $410.00 |
Mouse Ptpn1 encodes protein tyrosine phosphatase 1B (PTP1B), an ER-associated phosphatase that dephosphorylates receptor tyrosine kinases and key signaling intermediates to constrain growth factor and cytokine responses. PTP1B is a central negative regulator of insulin receptor and leptin receptor signaling, shaping PI3K–AKT and MAPK pathway dynamics and downstream metabolic gene expression. Through modulation of JAK/STAT and receptor phosphorylation states, PTP1B influences inflammatory signaling, cell adhesion, and stress responses. Dysregulated Ptpn1/PTP1B activity is widely studied in the context of insulin resistance, obesity-linked metabolic dysfunction, and cancer-relevant signaling rewiring, supporting its use in pathway dissection and genotype–phenotype studies in mouse models.
PTP1B Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ptpn1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ptpn1. 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 Ptpn1 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 Ptpn1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.