dendrin CRISPR Activation Plasmid (h): sc-404856-ACT

Human DDN encodes dendrin, a postsynaptic density–associated protein enriched in neurons and implicated in organizing synaptic signaling complexes. Dendrin participates in activity-dependent remodeling of dendritic spines and is linked to cytoskeletal regulation and protein–protein interactions that shape synaptic plasticity. Beyond the CNS, dendrin has been studied in glomerular podocytes, where it localizes to slit diaphragm–associated compartments and has been connected to pathways that influence cell structure and stress responses. Dysregulation of dendrin expression or localization has been investigated in the context of neuropsychiatric phenotypes and kidney injury–associated processes, supporting its value as a research target for mechanisms of synapse and filtration barrier integrity.

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

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

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