SVEP1 CRISPR Activation Plasmid (h): sc-413315-ACT

SVEP1 (sushi, von Willebrand factor type A, EGF and pentraxin domain containing 1) encodes a large extracellular matrix-associated glycoprotein that supports cell–cell and cell–matrix interactions. It participates in adhesion and morphogenetic processes by modulating integrin-dependent signaling, extracellular matrix organization, and tissue remodeling programs that influence endothelial–stromal crosstalk. SVEP1 has been implicated in developmental and vascular biology contexts, and altered expression has been associated with inflammatory remodeling and cardiometabolic disease susceptibility. These properties make SVEP1 a useful target for studying extracellular matrix signaling networks, cell migration, and microenvironment-dependent regulation of gene expression.

SVEP1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SVEP1 expression without altering the underlying DNA sequence.

SVEP1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SVEP1 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the SVEP1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SVEP1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SVEP1 locus and enabling the study of SVEP1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SVEP1 pathway restoration in tumor cells with silenced or reduced SVEP1 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.