CTHRC1 Double Nickase Plasmid (m2): sc-427107-NIC-2
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CTHRC1 Double Nickase Plasmid (m2) 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
- CTHRC1 Double Nickase Plasmid (m2) and CTHRC1 Double Nickase Plasmid (m22) encode distinct paired gRNA designs targeting Cthrc1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CTHRC1 Double Nickase Plasmid (m2) | sc-427107-NIC-2 | 20 µg | $410.00 |
Mouse Cthrc1 encodes CTHRC1, a secreted extracellular matrix–associated protein that modulates tissue remodeling by influencing collagen deposition and cell–matrix interactions. CTHRC1 is commonly linked to regulation of non-canonical and canonical Wnt signaling, impacting cell migration, adhesion dynamics, and vascular or stromal responses during development and repair. Altered Cthrc1 expression has been implicated in fibrotic remodeling and tumor-associated microenvironment changes, making it a useful target for dissecting mechanisms of invasion, metastasis-supportive stroma, and pathological matrix turnover. Gene editing of Cthrc1 in mouse models or cultured cells supports functional studies of extracellular matrix signaling, wound-healing–like programs, and pathway crosstalk in inflammation-driven remodeling contexts.
CTHRC1 Double Nickase Plasmid (m2) consists of a matched pair of plasmids engineered for high-specificity editing of the Cthrc1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cthrc1. 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 Cthrc1 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 Cthrc1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.