GCP-2 Double Nickase Plasmid (m): sc-422852-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GCP-2 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
- GCP-2 Double Nickase Plasmid (m) and GCP-2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Cxcl5. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GCP-2 Double Nickase Plasmid (m) | sc-422852-NIC | 20 µg | $410.00 |
Cxcl5 encodes granulocyte chemotactic protein-2 (GCP-2), a secreted ELR+ CXC chemokine that coordinates innate immune recruitment by promoting neutrophil chemotaxis and activation through CXCR2 signaling. In mouse tissues, GCP-2 contributes to inflammatory cell trafficking, epithelial–stromal communication, and angiogenic responses, integrating with NF-κB–regulated cytokine networks and chemokine gradients that shape leukocyte extravasation. Perturbation of Cxcl5 expression is commonly linked to dysregulated inflammatory milieus, altered neutrophil-driven tissue injury, and microenvironmental remodeling observed in models of infection, chronic inflammation, and tumor-associated inflammation. As a node in chemokine signaling pathways, Cxcl5 is frequently studied for its role in myeloid recruitment, cytokine crosstalk, and effects on barrier tissues such as lung and gastrointestinal epithelium.
GCP-2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cxcl5 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cxcl5. 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 Cxcl5 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 Cxcl5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.