CDCP1 Double Nickase Plasmid (h): sc-404730-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CDCP1 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
- CDCP1 Double Nickase Plasmid (h) and CDCP1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDCP1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CDCP1 Antibody (D-1): sc-515545
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CDCP1 Double Nickase Plasmid (h) | sc-404730-NIC | 20 µg | $410.00 |
CDCP1 (CUB domain-containing protein 1) is a transmembrane glycoprotein implicated in cell adhesion dynamics, migration, and survival signaling in epithelial-derived cells. It functions as a signaling scaffold that can be phosphorylated by Src family kinases and engage PKCδ and other downstream effectors, linking extracellular cues to cytoskeletal remodeling. CDCP1 activity intersects with pathways controlling anoikis resistance, integrin-associated signaling, and membrane trafficking, making it relevant to studies of invasion, metastatic dissemination, and stress-adaptive responses. Dysregulated CDCP1 expression and phosphorylation have been associated with aggressive tumor phenotypes and altered cell–matrix interactions across multiple cancer contexts.
CDCP1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDCP1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDCP1. 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 CDCP1 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 CDCP1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.