PIG-G Double Nickase Plasmid (h): sc-412361-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PIG-G 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
- PIG-G Double Nickase Plasmid (h) and PIG-G Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting PIGG. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PIG-G Double Nickase Plasmid (h) | sc-412361-NIC | 20 µg | $410.00 | |||
PIG-G Double Nickase Plasmid (h2) | sc-412361-NIC-2 | 20 µg | $410.00 |
PIGG encodes the human PIG-G protein, an essential component of the glycosylphosphatidylinositol (GPI) anchor biosynthetic machinery in the endoplasmic reticulum. PIG-G functions within the GPI transamidase/transferase-associated pathway that enables attachment of preassembled GPI anchors to nascent proteins, supporting correct membrane localization of many cell-surface and secreted proteins. Disruption of GPI-anchor assembly perturbs trafficking and stability of GPI-anchored proteins, influencing processes such as cell signaling, adhesion, and immune recognition. Genetic defects in GPI-anchor biosynthesis, including variants affecting PIGG, are linked to inherited GPI deficiency syndromes characterized by neurodevelopmental phenotypes, making PIGG a useful node for mechanistic studies of membrane-anchoring and proteostasis.
PIG-G Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the PIGG locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within PIGG. 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 PIGG 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 PIGG-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.