Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
TIMP-2 CRISPR Activation Plasmid (h): sc-400685-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TIMP-2 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- TIMP-2 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by TIMP-2 CRISPR Activation Plasmid (h) and TIMP-2 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the TIMP2 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TIMP-2 Antibody (3A4): sc-21735
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TIMP-2 CRISPR Activation Plasmid (h) | sc-400685-ACT | 20 µg | $397.00 |
Human TIMP2 encodes tissue inhibitor of metalloproteinases-2 (TIMP-2), a secreted regulator of extracellular matrix turnover that modulates the activity of matrix metalloproteinases, including inhibition of MMP2, and shapes protease-dependent remodeling. By balancing metalloproteinase-driven matrix degradation with inhibition, TIMP-2 influences cell migration, adhesion, and tissue architecture, linking it to pathways that govern invasion, angiogenesis, and wound repair. TIMP-2 also participates in controlling pericellular proteolysis through interactions with membrane-associated factors such as MT1-MMP, thereby impacting signaling cues in the tumor microenvironment and fibrotic remodeling. Dysregulated TIMP2 expression has been associated with altered ECM dynamics observed across cancer biology, inflammatory states, and connective tissue disorders, making it a useful node for mechanistic studies of matrix-dependent phenotypes.
TIMP-2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TIMP2 expression without altering the underlying DNA sequence.
TIMP-2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TIMP2 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 TIMP2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TIMP-2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TIMP2 locus and enabling the study of TIMP-2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TIMP-2 pathway restoration in tumor cells with silenced or reduced TIMP2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.