TARSL1 Lentiviral Activation Particles (h): sc-410152-LAC

TARS2 encodes the mitochondrial threonyl‑tRNA synthetase TARSL1, an aminoacyl‑tRNA ligase required for charging mitochondrial tRNAThr and sustaining translation of oxidative phosphorylation (OXPHOS) subunits encoded by mtDNA. By supporting mitochondrial protein synthesis, TARSL1 contributes to respiratory chain assembly, ATP production, and integrated mitochondrial stress responses that modulate metabolism and cell fate decisions. Perturbation of mitochondrial translation is closely linked to impaired bioenergetics, altered redox homeostasis, and activation of compensatory signaling pathways, making TARS2/TARSL1 function relevant to studies of mitochondrial dysfunction in neurodegeneration, cardiometabolic disease, and cancer metabolism. As a core component of mitochondrial gene expression, TARSL1 also provides a mechanistic entry point for investigating mitonuclear communication and translational control in human cells.

TARSL1 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 TARS2 upregulation across a broader range of human cell types.

TARSL1 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 TARS2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous TARSL1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TARS2 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.