GSK3 beta Double Nickase Plasmid (h): sc-400090-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GSK3 beta 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
- GSK3 beta Double Nickase Plasmid (h) and GSK3 beta Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GSK3B. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: GSK3 beta Antibody (E-11): sc-377213
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GSK3 beta Double Nickase Plasmid (h) | sc-400090-NIC | 20 µg | $410.00 | |||
GSK3 beta Double Nickase Plasmid (h2) | sc-400090-NIC-2 | 20 µg | $410.00 |
Human GSK3B encodes glycogen synthase kinase-3 beta (GSK3 beta), a constitutively active serine/threonine kinase that integrates cues from growth factor, metabolic, and stress signaling. GSK3 beta is a key node in PI3K–AKT signaling and Wnt/β-catenin regulation, influencing phosphorylation-dependent control of glycogen metabolism, cell cycle progression, apoptosis, and differentiation. Through modulation of transcription factors and cytoskeletal regulators, it shapes pathways governing neuronal function, insulin responsiveness, and inflammatory signaling. Dysregulated GSK3B activity and Wnt/AKT pathway imbalance are frequently studied in cancer biology, neurodegeneration, and metabolic disease mechanisms.
GSK3 beta Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GSK3B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GSK3B. 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 GSK3B 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 GSK3B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.