Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
AMPK alpha 2 CRISPR Activation Plasmid (h): sc-400277-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- AMPK alpha 2 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- AMPK alpha 2 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by AMPK alpha 2 CRISPR Activation Plasmid (h) and AMPK alpha 2 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the PRKAA2 transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
AMPK alpha 2 CRISPR Activation Plasmid (h) | sc-400277-ACT | 20 µg | $397.00 | |||
AMPK alpha 2 CRISPR Activation Plasmid (h2) | sc-400277-ACT-2 | 20 µg | $397.00 |
PRKAA2 encodes the catalytic α2 subunit of AMP-activated protein kinase (AMPK), a central energy sensor that maintains cellular ATP homeostasis in response to metabolic stress. AMPKα2 integrates upstream signals from LKB1 and CaMKK2 to regulate glucose uptake, lipid oxidation, mitochondrial biogenesis, and autophagy through pathways including mTORC1 inhibition and ULK1 activation. In human tissues, AMPKα2 activity is closely linked to nutrient sensing and redox balance, with broad relevance to metabolic dysregulation, inflammation, and stress-adaptation phenotypes observed across cardiometabolic and neurodegeneration-associated contexts. Modulating PRKAA2 expression is therefore useful for dissecting how energy stress signaling reshapes transcriptional programs and cell fate decisions.
AMPK alpha 2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PRKAA2 expression without altering the underlying DNA sequence.
AMPK alpha 2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PRKAA2 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the PRKAA2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous AMPK alpha 2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PRKAA2 locus and enabling the study of AMPK alpha 2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of AMPK alpha 2 pathway restoration in tumor cells with silenced or reduced PRKAA2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.