PRIC285 Double Nickase Plasmid (h): sc-406441-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PRIC285 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
- PRIC285 Double Nickase Plasmid (h) and PRIC285 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HELZ2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PRIC285 Double Nickase Plasmid (h) | sc-406441-NIC | 20 µg | $410.00 |
HELZ2 (also reported as PRIC285) encodes a helicase-like transcriptional co-regulator implicated in coupling nuclear receptor signaling to gene expression programs that control lipid handling and inflammatory responses. It participates in transcriptional control downstream of receptors such as PPARs and related metabolic regulators, influencing pathways linked to adipogenesis, insulin sensitivity, and innate immune signaling. Altered HELZ2/PRIC285 activity has been associated with dysregulated metabolic homeostasis and inflammatory phenotypes, supporting its use as a mechanistic node connecting metabolism and transcriptional regulation. These functions make HELZ2 a relevant target for studying gene regulatory networks in hepatocytes, adipocytes, and immune-derived cell models.
PRIC285 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HELZ2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HELZ2. 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 HELZ2 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 HELZ2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.