WISP-1 Double Nickase Plasmid (m): sc-423705-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- WISP-1 Double Nickase Plasmid (m) 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
- WISP-1 Double Nickase Plasmid (m) and WISP-1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Wisp1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
WISP-1 Double Nickase Plasmid (m) | sc-423705-NIC | 20 µg | $410.00 | |||
WISP-1 Double Nickase Plasmid (m2) | sc-423705-NIC-2 | 20 µg | $410.00 |
Wisp1 (WISP-1; CCN4) encodes a secreted matricellular protein that integrates extracellular matrix cues with growth factor signaling to regulate cell adhesion, migration, and proliferation in mouse tissues. WISP-1 is commonly linked to Wnt/β-catenin signaling and interfaces with integrin-mediated pathways that influence cytoskeletal remodeling, survival programs, and transcriptional responses during development and tissue remodeling. Altered WISP-1 expression has been associated with dysregulated fibrotic responses, abnormal angiogenic and inflammatory signaling, and tumor microenvironment remodeling in cancer-relevant models. These properties make WISP-1 a useful target for dissecting ECM–signal transduction crosstalk in stromal biology and disease-relevant remodeling processes.
WISP-1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Wisp1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Wisp1. 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 Wisp1 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 Wisp1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.