
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADAMTS-12 CRISPR Activation Plasmid (h) | sc-403884-ACT | 20 µg | $397.00 |
ADAMTS12 encodes ADAMTS-12, a secreted metalloproteinase of the ADAMTS family that remodels the extracellular matrix by processing proteoglycans and related matrix components. Through regulation of matrix turnover, cell–matrix adhesion, and tissue microenvironment dynamics, ADAMTS-12 influences pathways linked to development, inflammation, and stromal remodeling. Altered ADAMTS12 expression has been associated with changes in cartilage and connective tissue homeostasis and with tumor–stroma interactions in multiple cancer types. These properties make ADAMTS-12 a useful target for studying extracellular proteolysis, matrix-dependent signaling, and microenvironment-driven phenotypes.
ADAMTS-12 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ADAMTS12 expression without altering the underlying DNA sequence.
ADAMTS-12 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ADAMTS12 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 ADAMTS12 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ADAMTS-12 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ADAMTS12 locus and enabling the study of ADAMTS-12-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ADAMTS-12 pathway restoration in tumor cells with silenced or reduced ADAMTS12 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.