HYAL1 Double Nickase Plasmid (h): sc-404500-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HYAL1 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
- HYAL1 Double Nickase Plasmid (h) and HYAL1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HYAL1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: HYAL1 Antibody (1D10): sc-101340
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HYAL1 Double Nickase Plasmid (h) | sc-404500-NIC | 20 µg | $410.00 | |||
HYAL1 Double Nickase Plasmid (h2) | sc-404500-NIC-2 | 20 µg | $410.00 |
HYAL1 encodes hyaluronoglucosaminidase 1, a lysosomal endoglycosidase that degrades hyaluronan and other glycosaminoglycans to regulate extracellular matrix turnover and tissue hydration. By controlling hyaluronan catabolism, HYAL1 influences pericellular matrix organization, cell adhesion and migration, and signaling outputs linked to inflammation and stromal remodeling. Altered HYAL1 activity has been associated with dysregulated matrix degradation and remodeling phenotypes observed in cancer biology, fibrotic processes, and vascular pathology. HYAL1 is therefore widely studied in pathways connecting lysosomal glycan processing with microenvironment-dependent cell behavior.
HYAL1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HYAL1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HYAL1. 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 HYAL1 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 HYAL1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.