Akt2 Double Nickase Plasmid (m): sc-419072-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Akt2 Double Nickase Plasmid (m) 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 (m) and Akt2 Double Nickase Plasmid (m2) 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 (1G8C12): sc-81148
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Akt2 Double Nickase Plasmid (m) | sc-419072-NIC | 20 µg | $410.00 | |||
Akt2 Double Nickase Plasmid (m2) | sc-419072-NIC-2 | 20 µg | $410.00 |
Akt2 encodes the serine/threonine kinase AKT2, a central effector of PI3K signaling that couples growth factor and insulin receptor inputs to downstream control of glucose uptake, glycogen synthesis, lipid metabolism, and cell survival. In mouse tissues, AKT2 activity influences membrane trafficking of glucose transporters, mTORC1-regulated anabolic programs, and phosphorylation-dependent inhibition of pro-apoptotic factors such as FOXO family transcription factors. Dysregulated AKT2 signaling is associated with altered insulin sensitivity and metabolic homeostasis, and aberrant pathway activation is frequently examined in models of proliferation, stress responses, and oncogenic signaling. As a node integrating receptor tyrosine kinase cues with metabolic and cell-cycle circuitry, Akt2 is widely studied in adipocytes, hepatocytes, myocytes, and diverse cancer cell contexts.
Akt2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Akt2 locus in mouse 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.