
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PRELI Lentiviral Activation Particles (h) | sc-411975-LAC | 200 µl | $455.00 |
Human PRELID1 encodes PRELI, a mitochondrial intermembrane space protein that participates in intramitochondrial lipid trafficking and supports mitochondrial membrane architecture and bioenergetic homeostasis. PRELI functions in processes linked to phospholipid handling and cristae maintenance, influencing respiratory chain performance, redox balance, and susceptibility to mitochondrial stress. Altered PRELID1/PRELI regulation has been examined in contexts of mitochondrial dysfunction, where perturbed lipid composition and impaired oxidative phosphorylation can contribute to cellular vulnerability. These features make PRELI relevant to mechanistic studies of mitochondrial quality control, metabolic adaptation, and stress signaling pathways.
PRELI 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 PRELID1 upregulation across a broader range of human cell types.
PRELI 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 PRELID1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PRELI expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PRELID1 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.