GRO1 Double Nickase Plasmid (m): sc-420697-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GRO1 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
- GRO1 Double Nickase Plasmid (m) and GRO1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Cxcl1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: GRO1 Antibody (S-19): sc-80516
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GRO1 Double Nickase Plasmid (m) | sc-420697-NIC | 20 µg | $410.00 |
Mouse Cxcl1 encodes the chemokine GRO1 (also known as KC), a secreted ELR+ CXC chemokine that binds CXCR2 to promote neutrophil chemotaxis, adhesion, and activation at sites of tissue injury or infection. GRO1 signaling integrates with inflammatory cytokine networks and downstream pathways such as NF-κB and MAPK to shape leukocyte recruitment, endothelial responses, and local chemokine gradients. Dysregulated Cxcl1 expression is commonly studied in models of acute and chronic inflammation, tumor-associated myeloid infiltration, and tissue remodeling, where altered neutrophil trafficking can influence angiogenesis and microenvironmental signaling. These features make Cxcl1 a useful target for dissecting innate immune cell migration and inflammatory crosstalk in mouse systems.
GRO1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cxcl1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cxcl1. 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 Cxcl1 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 Cxcl1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.