ERBIN Double Nickase Plasmid (h): sc-402637-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ERBIN 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
- ERBIN Double Nickase Plasmid (h) and ERBIN Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ERBIN. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ERBIN Antibody (10D2): sc-293468
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ERBIN Double Nickase Plasmid (h) | sc-402637-NIC | 20 µg | $410.00 |
ERBIN (ERBB2-interacting protein) is a PDZ domain–containing scaffold that localizes to epithelial cell junctions and coordinates receptor and adhesion signaling. By interacting with ERBB2/HER2 and linking membrane complexes to downstream effectors, ERBIN helps shape MAPK/ERK and PI3K/AKT pathway output, polarity maintenance, and cytoskeletal organization. It also participates in the regulation of TGF-β/SMAD signaling and can influence inflammatory transcriptional programs in a context-dependent manner. Altered ERBIN expression or function has been associated with dysregulated growth factor signaling and barrier defects, supporting its relevance in models of cancer biology, epithelial homeostasis, and immune-related processes.
ERBIN Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ERBIN locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ERBIN. 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 ERBIN 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 ERBIN-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.