chordin Double Nickase Plasmid (h): sc-404997-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- chordin 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
- chordin Double Nickase Plasmid (h) and chordin Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CHRD. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
chordin Double Nickase Plasmid (h) | sc-404997-NIC | 20 µg | $410.00 | |||
chordin Double Nickase Plasmid (h2) | sc-404997-NIC-2 | 20 µg | $410.00 |
Human CHRD encodes chordin, a secreted extracellular matrix glycoprotein that antagonizes BMP signaling by binding BMP2/4/7 and limiting receptor engagement. By shaping BMP gradient formation and modulating SMAD1/5/9 phosphorylation outputs, chordin helps control dorsoventral patterning, mesoderm induction, and organogenesis, and remains relevant to pathways governing osteogenic and chondrogenic differentiation. Altered CHRD activity can perturb developmental signaling balance and has been studied in the context of congenital malformations and dysregulated tissue remodeling processes. In cultured systems, CHRD perturbation is commonly used to interrogate BMP pathway crosstalk with WNT and TGF-β signaling and to dissect extracellular regulation of morphogen availability.
chordin Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CHRD locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CHRD. 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 CHRD 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 CHRD-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.