BCAM Double Nickase Plasmid (h): sc-405080-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BCAM 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
- BCAM Double Nickase Plasmid (h) and BCAM Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BCAM. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: BCAM Antibody (D-6): sc-365191
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BCAM Double Nickase Plasmid (h) | sc-405080-NIC | 20 µg | $410.00 | |||
BCAM Double Nickase Plasmid (h2) | sc-405080-NIC-2 | 20 µg | $410.00 |
BCAM (basal cell adhesion molecule), also known as Lutheran blood group glycoprotein, is a cell-surface immunoglobulin superfamily member that mediates adhesion to laminin α5 in basement membranes. Through interactions with the extracellular matrix and cytoskeletal adaptors, BCAM influences cell–matrix attachment, migration, and mechanical signaling that shape epithelial and endothelial organization. Its expression and glycosylation status can modulate vascular and inflammatory cell trafficking and contribute to context-dependent changes in tissue integrity. Altered BCAM activity has been studied in relation to red blood cell adhesion phenomena, tumor cell invasiveness, and microenvironmental remodeling relevant to hematologic and solid-tumor biology.
BCAM Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BCAM locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BCAM. 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 BCAM 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 BCAM-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.