densin-180 CRISPR Activation Plasmid (h): sc-403589-ACT

LRRC7 encodes densin-180, a postsynaptic density scaffold enriched at excitatory synapses where it helps organize protein complexes that regulate dendritic spine architecture and synaptic signaling. Densin-180 associates with membrane and cytoskeletal components and integrates signaling pathways linked to synaptic plasticity, including interactions that couple receptor-associated machinery to downstream kinases and actin remodeling. Through its role in maintaining postsynaptic organization and neuronal connectivity, LRRC7 is studied in the context of neurodevelopmental and neuropsychiatric disease mechanisms where synapse structure and signaling are perturbed. Experimental modulation of LRRC7 expression supports mechanistic analyses of synaptic maturation, activity-dependent signaling, and network function in human neuronal models.

densin-180 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LRRC7 expression without altering the underlying DNA sequence.

densin-180 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LRRC7 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 LRRC7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous densin-180 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LRRC7 locus and enabling the study of densin-180-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of densin-180 pathway restoration in tumor cells with silenced or reduced LRRC7 expression.

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