GSKIP Double Nickase Plasmid (h): sc-412211-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GSKIP 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
- GSKIP Double Nickase Plasmid (h) and GSKIP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GSKIP. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GSKIP Double Nickase Plasmid (h) | sc-412211-NIC | 20 µg | $410.00 | |||
GSKIP Double Nickase Plasmid (h2) | sc-412211-NIC-2 | 20 µg | $410.00 |
GSKIP (GSK3β interaction protein) encodes a small scaffold protein that binds glycogen synthase kinase 3β and helps position this kinase within multiprotein signaling assemblies. Through modulation of GSK3-dependent phosphorylation events, GSKIP can influence pathways linked to Wnt/β-catenin signaling, cAMP/PKA signaling dynamics, and broader control of cell fate decisions, proliferation, and differentiation programs. Altered regulation of GSK3-centered networks is frequently connected to dysregulated growth and developmental phenotypes, making GSKIP a useful node for probing pathway cross-talk. As a human protein with roles in kinase scaffolding, GSKIP supports mechanistic studies of signaling specificity and compartmentalization in disease-relevant cellular contexts.
GSKIP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GSKIP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GSKIP. 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 GSKIP 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 GSKIP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.