β ig-h3 Double Nickase Plasmid (m): sc-423369-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- β ig-h3 Double Nickase Plasmid (m) 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
- β ig-h3 Double Nickase Plasmid (m) and β ig-h3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Tgfbi. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
β ig-h3 Double Nickase Plasmid (m) | sc-423369-NIC | 20 µg | $410.00 |
Tgfbi encodes β ig-h3 (TGFBI), a secreted extracellular matrix protein induced by TGF-β signaling that modulates cell–matrix adhesion, migration, and tissue remodeling through interactions with integrins and structural matrix components. In mouse systems, β ig-h3 contributes to extracellular matrix organization, wound repair–associated processes, and regulation of epithelial and stromal cell behavior, linking it to pathways such as focal adhesion signaling and TGF-β–driven fibrotic responses. Altered TGFBI expression or matrix deposition is frequently studied in contexts of pathological remodeling, including fibrosis-like phenotypes and tumor microenvironment changes, where ECM composition can influence invasion and immune cell trafficking. These features make Tgfbi a useful target for dissecting how TGF-β-regulated ECM proteins shape tissue architecture and mechanobiology.
β ig-h3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Tgfbi locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Tgfbi. 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 Tgfbi 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 Tgfbi-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.