Prohibitin Lentiviral Activation Particles (h): sc-416271-LAC

PHB encodes prohibitin, a highly conserved scaffold protein enriched in mitochondria and other membrane compartments that helps regulate mitochondrial biogenesis, inner membrane organization, and proteostasis through chaperone-like functions. Prohibitin participates in control of cell-cycle progression and apoptosis and interfaces with signaling networks such as MAPK/ERK and PI3K/AKT, influencing transcriptional programs and stress responses. Altered PHB expression or localization has been linked to disrupted oxidative phosphorylation, elevated reactive oxygen species handling defects, and changes in epithelial-to-mesenchymal and proliferative states. These properties make PHB a widely studied node in mitochondrial quality control, cell fate regulation, and disease-associated metabolic remodeling in human cells.

Prohibitin 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 PHB upregulation across a broader range of human cell types.

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