Pdcd-1 Double Nickase Plasmid (h): sc-403008-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Pdcd-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
- Pdcd-1 Double Nickase Plasmid (h) and Pdcd-1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PDCD1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Pdcd-1 Double Nickase Plasmid (h) | sc-403008-NIC | 20 µg | $410.00 |
PDCD1 encodes Pdcd-1 (PD-1), an inhibitory immune checkpoint receptor expressed primarily on activated T cells, B cells, and myeloid subsets that attenuates antigen receptor signaling to maintain peripheral tolerance. Upon engagement by PD-L1 or PD-L2, Pdcd-1 recruits phosphatases such as SHP2 to dephosphorylate proximal signaling nodes, suppressing PI3K–AKT and RAS–MAPK pathways and reducing cytokine production, proliferation, and cytotoxic activity. PDCD1 regulation influences T cell exhaustion programs during chronic antigen exposure and shapes the tumor microenvironment by modulating effector function and immune surveillance. Dysregulated Pdcd-1 signaling is implicated in cancer immune evasion, persistent viral infection, and autoimmune phenotypes linked to altered tolerance checkpoints.
Pdcd-1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PDCD1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PDCD1. 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 PDCD1 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 PDCD1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.