HAS1 Double Nickase Plasmid (h): sc-401951-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HAS1 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
- HAS1 Double Nickase Plasmid (h) and HAS1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HAS1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HAS1 Double Nickase Plasmid (h) | sc-401951-NIC | 20 µg | $410.00 | |||
HAS1 Double Nickase Plasmid (h2) | sc-401951-NIC-2 | 20 µg | $410.00 |
HAS1 encodes hyaluronan synthase 1, a plasma membrane enzyme that polymerizes hyaluronan, a key extracellular matrix glycosaminoglycan regulating tissue hydration, viscoelasticity, and pericellular matrix organization. By controlling hyaluronan production, HAS1 influences cell adhesion, migration, and inflammatory signaling through hyaluronan–receptor interactions such as CD44- and RHAMM-linked pathways. Altered HAS1 expression or hyaluronan accumulation has been associated with stromal remodeling and dysregulated immune microenvironments in multiple disease contexts, making it relevant for studies of fibrosis, tumor–stroma interactions, and chronic inflammation. In cell models, perturbing HAS1 supports mechanistic dissection of extracellular matrix dynamics and hyaluronan-dependent signaling outputs.
HAS1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HAS1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HAS1. 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 HAS1 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 HAS1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.