mTOR Lentiviral Activation Particles (m): sc-425273-LAC

Mouse Mtor encodes the serine/threonine kinase mTOR, a master regulator of cellular growth that integrates amino acid availability, energy status, oxygen tension, and growth factor cues to coordinate anabolic and catabolic programs. As the catalytic core of mTORC1 and mTORC2, mTOR controls protein synthesis via S6K and 4E-BP1, lipid and nucleotide metabolism, autophagy suppression, and cytoskeletal organization through Akt/SGK signaling. mTOR signaling interfaces with PI3K–Akt, AMPK, TSC1/2–Rheb, and Rag GTPase pathways to balance proliferation, stress adaptation, and metabolic homeostasis. Dysregulated mTOR activity is widely studied in cancer biology, neurodevelopment and synaptic plasticity, immune cell activation, and metabolic disease models, providing a central node for mechanistic pathway interrogation in mouse systems.

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

mTOR Lentiviral Activation Particles (m) 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 Mtor transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous mTOR expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Mtor 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.