HIG2 Double Nickase Plasmid (h): sc-403510-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HIG2 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
- HIG2 Double Nickase Plasmid (h) and HIG2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HILPDA. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: HIG2 Antibody (G-2): sc-376704
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HIG2 Double Nickase Plasmid (h) | sc-403510-NIC | 20 µg | $410.00 |
HILPDA encodes hypoxia-inducible lipid droplet–associated protein (HIG2), a small protein that localizes to lipid droplets and is strongly induced by hypoxia and inflammatory cues. HIG2 supports cellular adaptation to low oxygen by promoting neutral lipid storage and remodeling fatty acid handling, linking HIF signaling to lipid droplet biogenesis and metabolic stress responses. This biology intersects with pathways controlling oxidative stress tolerance, nutrient deprivation, and innate immune activation, making HILPDA a useful node for studying hypoxia-driven metabolic reprogramming. Altered HILPDA expression has been reported in contexts of tumor hypoxia, macrophage polarization, and metabolic disease–associated inflammation, where lipid droplet dynamics can influence cell state and survival programs.
HIG2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HILPDA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HILPDA. 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 HILPDA 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 HILPDA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.