Vasohibin-2 Lentiviral Activation Particles (h): sc-407838-LAC

VASH2 encodes vasohibin-2, a secreted and cell-associated regulator of angiogenesis that modulates endothelial sprouting, vessel maturation, and microenvironmental remodeling. It participates in pathways governing extracellular matrix dynamics, cell migration, and paracrine signaling between stromal and vascular compartments, with downstream effects on hypoxia-adaptive and pro-angiogenic transcriptional programs. Altered VASH2 expression has been associated with tumor vascularization and invasive phenotypes in multiple cancer contexts, and it is also studied in inflammation-associated tissue remodeling. These properties make VASH2 a useful node for investigating angiogenic signaling, endothelial–tumor crosstalk, and microenvironment-driven disease mechanisms.

Vasohibin-2 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 VASH2 upregulation across a broader range of human cell types.

Vasohibin-2 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 VASH2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Vasohibin-2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native VASH2 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.