Osteoglycin CRISPR Activation Plasmid (h): sc-403018-ACT

OGN encodes osteoglycin, a small leucine-rich proteoglycan of the extracellular matrix that binds collagen fibrils and modulates matrix assembly, tissue tensile strength, and cell–matrix signaling. Osteoglycin influences growth factor availability and receptor signaling in stromal compartments, linking extracellular matrix remodeling to cellular programs such as adhesion, migration, and differentiation. Altered OGN expression has been associated with fibrotic remodeling and dysregulated extracellular matrix turnover, and it is frequently examined in contexts such as cardiovascular remodeling, tumor stroma biology, and wound repair. These functions make OGN a useful target for dissecting how matrix composition and organization shape tissue homeostasis and disease-associated microenvironments.

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

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

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