NDUFS1 Lentiviral Activation Particles (h): sc-416401-LAC

NDUFS1 encodes an essential core subunit of mitochondrial complex I (NADH:ubiquinone oxidoreductase) that supports oxidative phosphorylation by transferring electrons from NADH to ubiquinone and contributing to proton pumping across the inner mitochondrial membrane. Through its role in the electron transport chain, NDUFS1 influences cellular ATP production, mitochondrial membrane potential maintenance, and redox homeostasis, with downstream effects on reactive oxygen species signaling and metabolic adaptation. Perturbation of complex I function is linked to mitochondrial dysfunction phenotypes that impact energy-demanding tissues and can modulate susceptibility to oxidative stress. As a nuclear-encoded mitochondrial gene, NDUFS1 is widely studied in bioenergetics, mitochondrial quality control, and disease-relevant models of respiratory chain impairment.

NDUFS1 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 NDUFS1 upregulation across a broader range of human cell types.

NDUFS1 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 NDUFS1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous NDUFS1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native NDUFS1 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.