CELSR3 Double Nickase Plasmid (h): sc-405116-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CELSR3 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
- CELSR3 Double Nickase Plasmid (h) and CELSR3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CELSR3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CELSR3 Antibody (2F7): sc-293381
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CELSR3 Double Nickase Plasmid (h) | sc-405116-NIC | 20 µg | $410.00 | |||
CELSR3 Double Nickase Plasmid (h2) | sc-405116-NIC-2 | 20 µg | $410.00 |
CELSR3 encodes cadherin EGF LAG seven-pass G-type receptor 3, an atypical cadherin that functions as an adhesion GPCR at the cell surface. It participates in planar cell polarity signaling and contact-dependent communication that shapes tissue polarity, neuronal migration, and axon guidance during development. Through interactions with core PCP components and cytoskeletal regulators, CELSR3 contributes to coordinated cell orientation and neurite patterning. Altered CELSR3 expression or regulation has been associated with neurodevelopmental phenotypes and has been explored in cancer-related contexts where polarity and cell–cell adhesion influence invasion and tumor architecture.
CELSR3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CELSR3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CELSR3. 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 CELSR3 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 CELSR3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.