
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NP1 CRISPR Activation Plasmid (h) | sc-404189-ACT | 20 µg | $397.00 |
Neuronal pentraxin 1 (NPTX1; NP1) is a secreted synaptic protein enriched in the nervous system that participates in activity-dependent synapse remodeling and excitatory circuit regulation. NP1 associates with neuronal pentraxin complexes and contributes to clustering and stabilization of glutamatergic synapses, influencing AMPA receptor trafficking and synaptic maturation. Through these functions, NPTX1 is linked to pathways governing neuronal plasticity, neurite outgrowth, and network homeostasis. Altered NPTX1 expression has been reported in studies of neurodegeneration and neuropsychiatric biology, making it a useful target for mechanistic investigations of synaptic dysfunction.
NP1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous NPTX1 expression without altering the underlying DNA sequence.
NP1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the NPTX1 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 NPTX1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous NP1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native NPTX1 locus and enabling the study of NP1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of NP1 pathway restoration in tumor cells with silenced or reduced NPTX1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.