Gas1 Double Nickase Plasmid (h): sc-404384-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Gas1 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
- Gas1 Double Nickase Plasmid (h) and Gas1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GAS1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Gas1 Double Nickase Plasmid (h) | sc-404384-NIC | 20 µg | $410.00 | |||
Gas1 Double Nickase Plasmid (h2) | sc-404384-NIC-2 | 20 µg | $410.00 |
Growth arrest specific 1 (GAS1) encodes Gas1, a glycosylphosphatidylinositol-anchored cell-surface protein that modulates developmental signaling and cell-cycle control. Gas1 can influence Hedgehog pathway activity by affecting ligand–receptor interactions and signal propagation at the plasma membrane, linking extracellular cues to transcriptional programs governing proliferation and differentiation. Through these roles, GAS1 is commonly studied in contexts such as embryonic patterning, neurodevelopment, and tissue homeostasis. Altered GAS1 expression or signaling has been associated with dysregulated growth control in cancer biology and with congenital developmental phenotypes, making it relevant for mechanistic studies of pathway perturbation.
Gas1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GAS1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GAS1. 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 GAS1 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 GAS1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.