Peg10 Lentiviral Activation Particles (h): sc-406028-LAC

Human PEG10 encodes Peg10, a domesticated retrotransposon-derived gag/pol-like protein that supports RNA binding and post-transcriptional regulation, with prominent roles in cell growth, survival, and lineage programs. Peg10 activity intersects with ubiquitin-mediated proteostasis, cell cycle control, and signaling networks that shape proliferation and differentiation, including contexts such as placental development. Dysregulated PEG10 expression has been associated with altered apoptotic thresholds and invasive phenotypes across multiple disease-relevant models, making it a useful node for studying transcriptional control and oncogenic stress responses. In biomedical research, PEG10 serves as a tractable target to interrogate endogenous gene activation effects on cellular state, pathway engagement, and downstream transcriptomic remodeling.

Peg10 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 PEG10 upregulation across a broader range of human cell types.

Peg10 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 PEG10 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Peg10 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PEG10 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.