Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
PSGL-1 Double Nickase Plasmid (h): sc-401534-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PSGL-1 Double Nickase Plasmid (h) 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
- PSGL-1 Double Nickase Plasmid (h) and PSGL-1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SELPLG. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: PSGL-1 Antibody (KPL1): sc-13535
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PSGL-1 Double Nickase Plasmid (h) | sc-401534-NIC | 20 µg | $410.00 | |||
PSGL-1 Double Nickase Plasmid (h2) | sc-401534-NIC-2 | 20 µg | $410.00 |
SELPLG encodes P-selectin glycoprotein ligand-1 (PSGL-1), a mucin-like, sialylated and fucosylated cell-surface glycoprotein expressed on most leukocytes that mediates tethering and rolling on activated endothelium via binding to P-, E-, and L-selectins. Through its role in selectin-dependent adhesion, PSGL-1 coordinates early steps of leukocyte recruitment, transmigration, and inflammatory cell trafficking, integrating with chemokine signaling and integrin activation to stabilize leukocyte-endothelial interactions. PSGL-1 also participates in leukocyte-platelet crosstalk and can influence downstream immune activation programs by modulating cell contact-dependent signaling. Dysregulated PSGL-1–selectin biology is implicated in chronic inflammatory disorders, vascular inflammation, thrombosis-associated leukocyte recruitment, and cancer-associated metastasis research contexts, making SELPLG a useful target for mechanistic studies of adhesion and immune regulation.
PSGL-1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SELPLG locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SELPLG. 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 SELPLG 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 SELPLG-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.