neuroligin 2 CRISPR Activation Plasmid (h): sc-402250-ACT

Human NLGN2 encodes neuroligin 2, a postsynaptic cell-adhesion protein enriched at inhibitory synapses where it coordinates synapse specification, maturation, and neurotransmission by coupling to neurexins and scaffolding complexes such as gephyrin. Through these interactions, neuroligin 2 influences GABAergic synaptic assembly, receptor clustering, and excitation–inhibition balance, shaping network synchrony and plasticity. Dysregulation of NLGN2 expression or synaptic localization has been associated with altered inhibitory circuit function implicated in neurodevelopmental and neuropsychiatric phenotypes, including autism spectrum disorder, schizophrenia, and anxiety-related behaviors. As a synaptic organizer, NLGN2 is frequently studied in pathways governing interneuron connectivity, inhibitory synapse stability, and activity-dependent remodeling.

neuroligin 2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous NLGN2 expression without altering the underlying DNA sequence.

neuroligin 2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the NLGN2 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 NLGN2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous neuroligin 2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native NLGN2 locus and enabling the study of neuroligin 2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of neuroligin 2 pathway restoration in tumor cells with silenced or reduced NLGN2 expression.

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