HtrA4 Double Nickase Plasmid (h): sc-410377-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HtrA4 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
- HtrA4 Double Nickase Plasmid (h) and HtrA4 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HTRA4. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HtrA4 Double Nickase Plasmid (h) | sc-410377-NIC | 20 µg | $410.00 | |||
HtrA4 Double Nickase Plasmid (h2) | sc-410377-NIC-2 | 20 µg | $410.00 |
HTRA4 encodes HtrA4, a secreted serine protease of the HtrA family that contributes to extracellular protein quality control by cleaving misfolded or damaged proteins and modulating cell–matrix interactions. Through proteolysis of specific substrates, HtrA4 can influence stress-responsive signaling, inflammatory cascades, and remodeling processes that shape tissue homeostasis. Altered HTRA4 expression has been reported in contexts involving placental biology and vascular function, and dysregulation of extracellular protease activity is relevant to disease mechanisms linked to aberrant proteostasis and microenvironment remodeling. These features make HtrA4 a useful target for studying how secreted proteases tune signaling and structural dynamics in human cell systems.
HtrA4 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HTRA4 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HTRA4. 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 HTRA4 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 HTRA4-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.