CD362/SDC2/Syndecan-2 CRISPR Activation Plasmid (h): sc-401392-ACT

SDC2 encodes syndecan-2 (CD362), a transmembrane heparan sulfate proteoglycan that organizes the pericellular matrix and functions as a co-receptor for growth factors, chemokines, and extracellular matrix ligands. By coordinating interactions with integrins, Src family kinases, and Rho GTPase signaling, syndecan-2 modulates focal adhesion dynamics, cytoskeletal remodeling, and cell migration, with downstream effects on pathways such as FAK/ERK and Wnt/β-catenin. SDC2 also contributes to cell–cell communication and protease activity through ectodomain shedding, influencing angiogenic and inflammatory microenvironments. Dysregulated SDC2 expression has been associated with tumor cell invasion, fibrosis-related remodeling, and altered stromal signaling, supporting its use as a mechanistic node in disease-relevant signaling studies.

CD362/SDC2/Syndecan-2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SDC2 expression without altering the underlying DNA sequence.

CD362/SDC2/Syndecan-2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SDC2 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 SDC2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD362/SDC2/Syndecan-2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SDC2 locus and enabling the study of CD362/SDC2/Syndecan-2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD362/SDC2/Syndecan-2 pathway restoration in tumor cells with silenced or reduced SDC2 expression.

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