ADAMTS-7 CRISPR Activation Plasmid (h): sc-403381-ACT

ADAMTS7 encodes ADAMTS-7, a secreted zinc-dependent metalloproteinase of the ADAMTS family that remodels the extracellular matrix by processing proteoglycan substrates and regulating matrix turnover. Through its catalytic and ancillary domains, ADAMTS-7 influences cell–matrix interactions, tissue remodeling, and inflammatory signaling programs that shape vascular and connective tissue homeostasis. Altered ADAMTS7 expression or activity has been linked to pathways relevant to vascular smooth muscle cell migration and extracellular matrix remodeling, implicating it in mechanisms associated with atherosclerosis and coronary artery disease susceptibility. ADAMTS-7 is therefore widely studied in models of vascular injury, fibrosis-like remodeling, and matrix-driven signaling changes.

ADAMTS-7 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ADAMTS7 expression without altering the underlying DNA sequence.

ADAMTS-7 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ADAMTS7 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 ADAMTS7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ADAMTS-7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ADAMTS7 locus and enabling the study of ADAMTS-7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ADAMTS-7 pathway restoration in tumor cells with silenced or reduced ADAMTS7 expression.

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