PLAC8 Lentiviral Activation Particles (h): sc-405093-LAC

PLAC8 (placenta-associated 8), also known as Onzin, encodes a small cysteine-rich protein implicated in regulating cell differentiation, epithelial homeostasis, and stress-response signaling. In human cells, PLAC8 has been linked to modulation of proliferation and survival programs, including pathways associated with MAPK and PI3K/AKT signaling outputs, as well as processes tied to cytoskeletal organization and membrane dynamics. Altered PLAC8 expression has been reported across multiple tumor contexts and inflammatory states, where it correlates with changes in invasion, metabolic adaptation, and immune-associated phenotypes. These features make PLAC8 a useful target for dissecting transcriptional networks that control lineage decisions and microenvironment-responsive cell behaviors.

PLAC8 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 PLAC8 upregulation across a broader range of human cell types.

PLAC8 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 PLAC8 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PLAC8 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PLAC8 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.