ErbB3/HER3 Double Nickase Plasmid (m): sc-420219-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ErbB3/HER3 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
- ErbB3/HER3 Double Nickase Plasmid (m) and ErbB3/HER3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Erbb3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ErbB3/HER3 Antibody (G-4): sc-7390
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ErbB3/HER3 Double Nickase Plasmid (m) | sc-420219-NIC | 20 µg | $410.00 |
Erbb3 encodes the receptor tyrosine kinase ErbB3/HER3, a member of the EGFR/ErbB family that functions primarily through heterodimerization with kinases such as ERBB2 to initiate downstream signaling. Despite limited intrinsic kinase activity, ErbB3 provides multiple PI3K-binding motifs and is a key node in PI3K–AKT and MAPK pathway regulation, influencing proliferation, survival, differentiation, and epithelial development in mouse tissues. Ligand engagement (e.g., neuregulins) and receptor crosstalk shape cellular responses, making Erbb3 a common mechanistic focus in studies of receptor signaling integration. Dysregulated ErbB3/HER3 signaling is frequently examined in oncogenic pathway remodeling, therapy-adaptive signaling, and developmental phenotypes relevant to disease models.
ErbB3/HER3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Erbb3 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Erbb3. 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 Erbb3 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 Erbb3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.