EMMPRIN/CD147 CRISPR Activation Plasmid (h): sc-400589-ACT

Basigin (BSG), commonly known as EMMPRIN/CD147, is a broadly expressed immunoglobulin superfamily glycoprotein that modulates cell–cell interactions and extracellular matrix remodeling. CD147 promotes induction of matrix metalloproteinases and cooperates with monocarboxylate transporters to support lactate transport and metabolic adaptation, linking it to hypoxia responses, inflammation, and cell migration programs. It also functions as a signaling hub through interactions with cyclophilins and integrin-associated pathways, influencing adhesion and cytoskeletal dynamics. Dysregulated BSG/CD147 expression has been associated with tumor invasion and metastasis biology, vascular remodeling, and inflammatory tissue damage, making it a useful target for mechanistic studies of microenvironmental crosstalk.

EMMPRIN/CD147 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BSG expression without altering the underlying DNA sequence.

EMMPRIN/CD147 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BSG 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 BSG transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous EMMPRIN/CD147 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BSG locus and enabling the study of EMMPRIN/CD147-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of EMMPRIN/CD147 pathway restoration in tumor cells with silenced or reduced BSG expression.

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