Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
GROβ Double Nickase Plasmid (h): sc-416416-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GROβ 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
- GROβ Double Nickase Plasmid (h) and GROβ Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CXCL2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GROβ Double Nickase Plasmid (h) | sc-416416-NIC | 20 µg | $410.00 |
CXCL2 encodes the chemokine GROβ (CXCL2), a secreted CXC-family ligand that signals primarily through CXCR2 to promote chemotaxis, adhesion, and activation of neutrophils and other myeloid cells. GROβ is induced downstream of inflammatory transcriptional programs including NF-κB and MAPK signaling, linking pathogen sensing and cytokine cascades to leukocyte recruitment. It contributes to shaping the local inflammatory milieu by regulating endothelial interactions and coordinating innate immune cell trafficking. Dysregulated CXCL2/GROβ expression is associated with chronic inflammatory states and has been studied in contexts such as tissue injury, autoimmune inflammation, and tumor-associated myeloid cell infiltration.
GROβ Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CXCL2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CXCL2. 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 CXCL2 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 CXCL2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.