G3BP2 Double Nickase Plasmid (h): sc-403630-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- G3BP2 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
- G3BP2 Double Nickase Plasmid (h) and G3BP2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting G3BP2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
G3BP2 Double Nickase Plasmid (h) | sc-403630-NIC | 20 µg | $410.00 |
G3BP2 (G3BP stress granule assembly factor 2) is an RNA-binding protein that functions as a key nucleator of stress granules and a regulator of mRNA stability and translation during cellular stress. It participates in post-transcriptional gene control linked to MAPK and innate immune signaling, influencing how cells adapt to oxidative stress, viral infection, and proteotoxic conditions. Through interactions with RNA and ribonucleoprotein complexes, G3BP2 helps coordinate stress-responsive remodeling of the transcriptome and proteome. Dysregulated G3BP2 activity and stress granule dynamics have been studied in contexts including cancer biology, neurodegeneration, and host–pathogen responses, making it relevant for mechanistic studies of cell fate and inflammatory signaling.
G3BP2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the G3BP2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within G3BP2. 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 G3BP2 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 G3BP2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.