Perlecan Lentiviral Activation Particles (h): sc-400823-LAC

HSPG2 encodes perlecan, a large heparan sulfate proteoglycan of basement membranes and pericellular matrices that organizes extracellular matrix architecture and regulates cell–matrix adhesion. Through binding to growth factors such as FGF2, VEGF, and PDGF, perlecan modulates signaling networks including FGF/FGFR, VEGF, and integrin-dependent pathways that influence proliferation, migration, and angiogenesis. Perlecan also contributes to mechanotransduction and filtration barrier function in tissues such as cartilage, vasculature, and kidney glomeruli. Altered HSPG2 expression or perlecan structural changes are associated with extracellular matrix dysregulation observed in vascular disease, skeletal dysplasias, and tumor microenvironment remodeling, making it a relevant target for matrix biology studies.

Perlecan 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 HSPG2 upregulation across a broader range of human cell types.

Perlecan 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 HSPG2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Perlecan expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native HSPG2 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.