
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
VEGF-C Lentiviral Activation Particles (m) | sc-423667-LAC | 200 µl | $455.00 | |||
VEGF-C Lentiviral Activation Particles (m2) | sc-423667-LAC-2 | 200 µl | $455.00 |
Mouse Vegfc encodes VEGF-C, a secreted growth factor that signals primarily through VEGFR-3 (FLT4) and, after proteolytic processing, can also engage VEGFR-2 to regulate lymphatic endothelial cell proliferation, migration, and survival. VEGF-C is a central driver of lymphangiogenesis and lymphatic vessel remodeling, integrating cues from PI3K–AKT, MAPK/ERK, and PLCγ pathways to coordinate endothelial sprouting and maturation. Altered Vegfc expression is frequently studied in contexts of tissue edema, inflammation, wound repair, and tumor-associated lymphatic remodeling, where changes in lymphatic drainage and immune cell trafficking influence disease biology.
VEGF-C 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 Vegfc upregulation across a broader range of human cell types.
VEGF-C 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 Vegfc transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous VEGF-C expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Vegfc 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.