AMPK alpha 1 Lentiviral Activation Particles (h): sc-400104-LAC

PRKAA1 encodes the catalytic AMPK alpha 1 subunit, a central energy sensor that couples changes in cellular AMP/ADP:ATP ratios to phosphorylation programs that restore metabolic homeostasis. AMPK alpha 1 regulates glucose uptake and glycolysis, fatty-acid oxidation, mitochondrial biogenesis, and autophagy through signaling axes that intersect with mTORC1, ULK1, ACC, and PGC-1–linked transcriptional networks. By integrating nutrient, hypoxia, and stress inputs, PRKAA1 helps coordinate cell growth decisions, redox balance, and proteostasis. Dysregulated AMPK signaling is implicated in metabolic disease phenotypes and is widely studied in the context of cancer cell metabolism, inflammation, and neurodegeneration as researchers probe context-dependent roles in stress adaptation.

AMPK alpha 1 Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient PRKAA1 upregulation across a broader range of human cell types.

AMPK alpha 1 Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the PRKAA1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous AMPK alpha 1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PRKAA1 genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.