neuroligin 1 CRISPR Activation Plasmid (h): sc-401668-ACT

Human NLGN1 encodes neuroligin 1, a postsynaptic cell-adhesion protein that binds presynaptic neurexins to organize excitatory synapse formation, maturation, and stability. Neuroligin 1 scaffolds synaptic protein complexes and contributes to activity-dependent synaptic plasticity by coordinating receptor localization and downstream signaling that shapes neuronal connectivity. Through its role in synaptogenesis and circuit refinement, NLGN1 is frequently studied in pathways governing glutamatergic transmission and synaptic remodeling. Altered neuroligin–neurexin signaling and NLGN1 dysregulation have been investigated in the context of neurodevelopmental and neuropsychiatric disease mechanisms, including synaptic dysfunction phenotypes.

neuroligin 1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous NLGN1 expression without altering the underlying DNA sequence.

neuroligin 1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the NLGN1 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 NLGN1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous neuroligin 1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native NLGN1 locus and enabling the study of neuroligin 1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of neuroligin 1 pathway restoration in tumor cells with silenced or reduced NLGN1 expression.

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