
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MMP-12 CRISPR Activation Plasmid (h) | sc-401853-ACT | 20 µg | $397.00 | |||
MMP-12 CRISPR Activation Plasmid (h2) | sc-401853-ACT-2 | 20 µg | $397.00 |
Human MMP12 encodes matrix metalloproteinase-12 (MMP-12), a zinc-dependent endopeptidase that degrades extracellular matrix components such as elastin and modulates the pericellular proteolytic microenvironment. MMP-12 activity intersects with extracellular matrix remodeling, inflammatory signaling, and cell migration programs, influencing tissue architecture and leukocyte trafficking. Dysregulated MMP-12 expression has been associated with chronic inflammatory conditions and fibrosis-related remodeling, and it is frequently studied in the context of tumor microenvironment dynamics, invasion-associated matrix turnover, and macrophage-driven pathology.
MMP-12 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MMP12 expression without altering the underlying DNA sequence.
MMP-12 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MMP12 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 MMP12 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MMP-12 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MMP12 locus and enabling the study of MMP-12-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MMP-12 pathway restoration in tumor cells with silenced or reduced MMP12 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.