Akt2 Double Nickase Plasmid (h): sc-400060-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Akt2 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
- Akt2 Double Nickase Plasmid (h) and Akt2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting AKT2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Akt2 Antibody (F-7): sc-5270
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Akt2 Double Nickase Plasmid (h) | sc-400060-NIC | 20 µg | $410.00 | |||
Akt2 Double Nickase Plasmid (h2) | sc-400060-NIC-2 | 20 µg | $410.00 |
AKT2 encodes the serine/threonine kinase Akt2, a central effector of the PI3K–AKT signaling axis that couples receptor tyrosine kinase and insulin signaling to cellular metabolism, growth, and survival. Akt2 regulates glucose uptake and glycogen synthesis through phosphorylation of downstream substrates such as AS160/TBC1D4 and GSK3, and contributes to mTORC1 control via TSC2 and PRAS40. In human cells, AKT2 activity helps coordinate insulin-responsive metabolic programs and can modulate cell-cycle progression, apoptosis resistance, and stress responses. Altered AKT2 signaling has been implicated in metabolic dysfunction and in oncogenic pathway rewiring where PI3K/AKT pathway components are frequently dysregulated.
Akt2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the AKT2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within AKT2. 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 AKT2 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 AKT2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.