ITI-H3 Double Nickase Plasmid (h): sc-404269-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ITI-H3 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
- ITI-H3 Double Nickase Plasmid (h) and ITI-H3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ITIH3. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ITI-H3 Double Nickase Plasmid (h) | sc-404269-NIC | 20 µg | $410.00 | |||
ITI-H3 Double Nickase Plasmid (h2) | sc-404269-NIC-2 | 20 µg | $410.00 |
ITIH3 encodes inter-α-trypsin inhibitor heavy chain 3 (ITI-H3), an extracellular matrix–associated protein that contributes to stabilization of hyaluronan-rich matrices through covalent transfer reactions mediated by the inter-α-inhibitor system. By shaping pericellular matrix architecture, ITI-H3 influences cell adhesion, migration, and tissue remodeling processes that intersect with inflammatory signaling and wound-response pathways. Altered ITIH3 expression or matrix incorporation has been reported in contexts of fibrosis, chronic inflammation, and tumor microenvironment remodeling, supporting its value as a mechanistic node linking ECM dynamics to disease-associated phenotypes. In biomedical research, ITIH3 is commonly studied for its roles in stromal–epithelial interactions, barrier function, and extracellular protease regulation.
ITI-H3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ITIH3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ITIH3. 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 ITIH3 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 ITIH3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.