VEGF Lentiviral Activation Particles (m): sc-423665-LAC

Vegfa encodes vascular endothelial growth factor (VEGF), a secreted ligand that coordinates endothelial proliferation, migration, and survival to regulate developmental and pathological angiogenesis in mouse tissues. VEGF signaling primarily engages VEGFR2/KDR to activate PI3K–AKT, MAPK/ERK, and PLCγ–PKC cascades, integrating with hypoxia-inducible pathways such as HIF-1–dependent transcriptional control. Through these networks, Vegfa influences vascular permeability, extracellular matrix remodeling, and recruitment of supporting mural cells during vessel maturation. Dysregulated VEGF axis activity is implicated in models of tumor neovascularization, ischemia-driven revascularization, inflammatory tissue remodeling, and ocular neovascular processes, making Vegfa a central node for mechanistic vascular biology studies.

VEGF 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 Vegfa upregulation across a broader range of human cell types.

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