AMPK alpha 2 Double Nickase Plasmid (m): sc-430803-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AMPK alpha 2 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
- AMPK alpha 2 Double Nickase Plasmid (m) and AMPK alpha 2 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Prkaa2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AMPK alpha 2 Double Nickase Plasmid (m) | sc-430803-NIC | 20 µg | $410.00 |
Prkaa2 encodes the catalytic α2 subunit of AMP-activated protein kinase (AMPK), a central sensor of cellular energy status that is activated by increased AMP/ADP relative to ATP. AMPKα2 helps coordinate metabolic homeostasis by phosphorylating targets that promote glucose uptake, fatty acid oxidation, and autophagy while restraining anabolic processes such as lipid and protein synthesis, integrating signals across the LKB1 and CaMKK2 pathways and intersecting with mTOR and insulin signaling. In mouse tissues, AMPKα2 is particularly relevant to skeletal muscle and cardiac energy metabolism and contributes to adaptation to energetic stress and mitochondrial function. Dysregulation of AMPK signaling is widely studied in metabolic disease models, ischemia/stress responses, and inflammation-associated phenotypes, making Prkaa2 a common target for mechanistic studies.
AMPK alpha 2 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Prkaa2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Prkaa2. 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 Prkaa2 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 Prkaa2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.