SYND3/SDC3/Syndecan-3 CRISPR Activation Plasmid (h): sc-402392-ACT

Human SDC3 encodes syndecan-3 (SYND3), a transmembrane heparan sulfate proteoglycan that functions as a co-receptor for extracellular matrix and growth factor ligands to modulate cell adhesion, migration, and receptor signaling. Through its glycosaminoglycan chains and cytoplasmic PDZ-binding motif, SYND3 influences pathways linked to cytoskeletal organization and MAPK/PI3K signaling, shaping neuronal development, axon guidance, and synaptic plasticity. SYND3 also participates in inflammatory and metabolic regulation by tuning chemokine and growth factor availability at the cell surface. Dysregulated SDC3 expression or altered proteoglycan signaling has been associated with processes relevant to neurodevelopmental phenotypes, obesity-related energy balance, and tumor cell–microenvironment interactions.

SYND3/SDC3/Syndecan-3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SDC3 expression without altering the underlying DNA sequence.

SYND3/SDC3/Syndecan-3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SDC3 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 SDC3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SYND3/SDC3/Syndecan-3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SDC3 locus and enabling the study of SYND3/SDC3/Syndecan-3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SYND3/SDC3/Syndecan-3 pathway restoration in tumor cells with silenced or reduced SDC3 expression.

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