
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CTGF CRISPR Activation Plasmid (m) | sc-420359-ACT | 20 µg | $397.00 |
Connective tissue growth factor (CTGF, encoded by mouse Ctgf) is a secreted matricellular protein that integrates extracellular matrix (ECM) remodeling with cellular adhesion, migration, and proliferation programs. CTGF functions downstream of profibrotic cues such as TGF-β/SMAD signaling and interfaces with integrin, MAPK, and Hippo–YAP/TAZ pathways to modulate fibroblast activation, angiogenic responses, and wound repair. Dysregulated Ctgf expression is linked to pathological fibrosis and stromal remodeling in multiple tissues, and it is frequently studied in contexts of chronic inflammation, tissue scarring, and tumor microenvironment crosstalk.
CTGF CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Ctgf expression without altering the underlying DNA sequence.
CTGF CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Ctgf 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 Ctgf transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CTGF expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Ctgf locus and enabling the study of CTGF-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CTGF pathway restoration in tumor cells with silenced or reduced Ctgf expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.