AMPKβ1 Double Nickase Plasmid (m): sc-422398-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AMPKβ1 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
- AMPKβ1 Double Nickase Plasmid (m) and AMPKβ1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Prkab1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: AMPKβ1 Antibody (Z14): sc-100357
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AMPKβ1 Double Nickase Plasmid (m) | sc-422398-NIC | 20 µg | $410.00 | |||
AMPKβ1 Double Nickase Plasmid (m2) | sc-422398-NIC-2 | 20 µg | $410.00 |
Prkab1 encodes the β1 regulatory subunit of AMP-activated protein kinase (AMPK), a central energy sensor that coordinates cellular responses to changes in ATP demand. AMPKβ1 contributes to complex assembly, subcellular localization, and substrate selection, integrating upstream signals to regulate fatty acid oxidation, mitochondrial homeostasis, and autophagy through pathways including mTORC1 and ULK1. In mouse cells, AMPKβ1 supports metabolic adaptation in liver, adipose tissue, and muscle and influences inflammatory signaling and stress resilience. Dysregulated AMPK signaling has been linked to metabolic phenotypes such as insulin resistance and hepatic steatosis, as well as altered growth control relevant to cancer biology and neurodegeneration research.
AMPKβ1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Prkab1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Prkab1. 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 Prkab1 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 Prkab1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.