
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Peg1 Lentiviral Activation Particles (m) | sc-421634-LAC | 200 µl | $455.00 |
Mouse Mest, also known as Peg1, is an imprinted gene that encodes a hydrolase-like protein implicated in embryonic growth regulation, placental function, and postnatal metabolic homeostasis. Peg1 expression is closely tied to developmental patterning and adipose tissue biology, with reported roles in adipogenesis, energy balance, and tissue remodeling programs. Dysregulated Mest/Peg1 activity has been associated with altered fat accumulation, growth phenotypes, and epigenetic instability linked to imprinting control. As a lineage- and context-sensitive locus, Mest is frequently used to study imprinting mechanisms, developmental gene regulation, and metabolic pathway remodeling in mouse model systems.
Peg1 Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Mest upregulation across a broader range of human cell types.
Peg1 Lentiviral Activation Particles (m) 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 Mest transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Peg1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Mest 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.