SCAP Double Nickase Plasmid (h): sc-401474-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SCAP 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
- SCAP Double Nickase Plasmid (h) and SCAP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SCAP. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SCAP Double Nickase Plasmid (h) | sc-401474-NIC | 20 µg | $410.00 | |||
SCAP Double Nickase Plasmid (h2) | sc-401474-NIC-2 | 20 µg | $410.00 |
SCAP (SREBF chaperone) is an endoplasmic reticulum membrane protein that escorts SREBP transcription factors from the ER to the Golgi in response to sterol depletion, enabling proteolytic activation and nuclear transcription of lipid metabolic genes. Through its interaction with INSIG proteins, SCAP mediates feedback control of cholesterol and fatty acid biosynthesis and coordinates cellular lipid homeostasis with membrane biogenesis. This SCAP–SREBP axis influences ER stress responses, lipoprotein metabolism, and metabolic reprogramming, making SCAP a key node for studying dyslipidemia-linked biology and lipid-dependent growth signaling in human cells. Altered SCAP/SREBP activity is frequently examined in contexts of hepatic steatosis, atherosclerosis-relevant lipid handling, and cancer-associated lipogenesis.
SCAP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SCAP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SCAP. 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 SCAP 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 SCAP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.