syntenin-1 CRISPR Activation Plasmid (h): sc-416825-ACT

SDCBP encodes syntenin-1, a PDZ domain–containing adaptor that binds syndecans and diverse membrane receptors to organize signaling complexes at the plasma membrane and endosomal compartments. Syntenin-1 regulates endocytic trafficking, exosome biogenesis, and cytoskeletal dynamics, influencing cell adhesion, migration, and intercellular communication. Through interactions with pathways such as FAK/Src, PI3K–AKT, and integrin-associated signaling, it helps coordinate receptor recycling and downstream transcriptional responses. Altered SDCBP expression and syntenin-1–dependent vesicle signaling have been associated with tumor progression, metastasis-related phenotypes, and inflammatory microenvironment modulation, supporting its relevance in mechanistic studies of disease biology.

syntenin-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SDCBP expression without altering the underlying DNA sequence.

syntenin-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SDCBP 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 SDCBP transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous syntenin-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SDCBP locus and enabling the study of syntenin-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of syntenin-1 pathway restoration in tumor cells with silenced or reduced SDCBP expression.

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