GROα Double Nickase Plasmid (h): sc-403256-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GROα 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
- GROα Double Nickase Plasmid (h) and GROα Double Nickase Plasmid (h2) 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: GROα Antibody (G-7): sc-514065
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GROα Double Nickase Plasmid (h) | sc-403256-NIC | 20 µg | $410.00 | |||
GROα Double Nickase Plasmid (h2) | sc-403256-NIC-2 | 20 µg | $410.00 |
CXCL1 encodes the chemokine GROα, a secreted ELR+ CXC ligand that binds CXCR2 to promote chemotaxis and activation of neutrophils and other myeloid populations. GROα signaling contributes to inflammatory cell trafficking, endothelial activation, and angiogenic responses, integrating with cytokine networks downstream of NF-κB and MAPK pathways. In human tissues, dysregulated CXCL1 expression is linked to chronic inflammation and tumor-associated stromal signaling, where it can shape immune infiltration and microenvironmental remodeling. As a soluble mediator, GROα is commonly measured and manipulated to interrogate paracrine signaling, leukocyte recruitment, and inflammatory gene programs.
GROα Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CXCL1 locus in human 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.