plasminogen CRISPR Activation Plasmid (h): sc-401410-ACT

Human PLG encodes plasminogen, a liver-derived zymogen that is converted to plasmin to drive fibrinolysis and broad extracellular proteolysis. Through interactions with tissue- and urokinase-type plasminogen activators and plasmin inhibitors, plasminogen regulates clot resolution, extracellular matrix remodeling, and cell migration, intersecting with wound repair and inflammatory protease networks. Plasmin activity also influences pericellular proteolysis and growth factor bioavailability, linking PLG to vascular homeostasis and tissue remodeling pathways. Altered plasminogen function or regulation is associated with dysregulated fibrin clearance and protease imbalance in thrombotic and inflammatory disease contexts, supporting mechanistic studies in hemostasis and matrix biology.

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

plasminogen CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PLG 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 PLG transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous plasminogen expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PLG locus and enabling the study of plasminogen-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of plasminogen pathway restoration in tumor cells with silenced or reduced PLG expression.

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