Flt-4 Lentiviral Activation Particles (h): sc-400684-LAC

FLT4 encodes Flt-4 (VEGFR-3), a receptor tyrosine kinase primarily expressed in lymphatic endothelial cells that transduces VEGF-C and VEGF-D signals to regulate lymphangiogenesis, vascular permeability, and endothelial cell migration. Upon ligand binding, Flt-4 activates canonical PI3K–AKT, MAPK/ERK, and PLCγ signaling cascades that coordinate proliferation and survival programs during vascular development and tissue remodeling. Dysregulated FLT4 signaling is implicated in lymphatic malformations and altered tumor-associated lymphangiogenesis, and it is frequently studied in the context of metastasis biology and inflammatory microenvironments. As a pathway node connecting growth factor signaling to endothelial fate decisions, FLT4 is widely used as a marker and functional determinant in vascular and lymphatic system research.

Flt-4 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 FLT4 upregulation across a broader range of human cell types.

Flt-4 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 FLT4 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Flt-4 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native FLT4 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.