MAF1 Lentiviral Activation Particles (h): sc-418170-LAC

MAF1 is a conserved transcriptional repressor that couples nutrient and stress signaling to RNA polymerase III output, thereby modulating synthesis of tRNAs and other small noncoding RNAs required for protein translation capacity. Its activity is regulated by phosphorylation downstream of PI3K–AKT–mTOR and related pathways, enabling cells to adjust biosynthetic demand during growth, starvation, and stress responses. Through control of Pol III transcription and translational homeostasis, MAF1 influences cell growth, metabolic adaptation, and proteostasis programs. Dysregulation of Pol III activity and upstream mTOR signaling networks in which MAF1 participates is frequently studied in contexts such as oncogenic growth, metabolic disease biology, and stress-associated phenotypes.

MAF1 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 MAF1 upregulation across a broader range of human cell types.

MAF1 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 MAF1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MAF1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native MAF1 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.