
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Synapsin Ia/b CRISPR Activation Plasmid (h) | sc-401064-ACT | 20 µg | $397.00 |
SYN1 encodes synapsin Ia/b, a neuron-enriched phosphoprotein that associates with synaptic vesicles and actin filaments to regulate vesicle clustering, reserve pool maintenance, and activity-dependent neurotransmitter release. Synapsin Ia/b function is controlled by phosphorylation downstream of Ca2+-dependent signaling and cAMP/PKA and MAPK pathways, coupling neuronal activity to presynaptic vesicle mobilization and synaptic plasticity. Through its role in shaping presynaptic efficacy and network excitability, altered SYN1 regulation has been linked to neurodevelopmental and neuropsychiatric phenotypes, including epilepsy and autism spectrum disorder, and is frequently studied in models of synaptic dysfunction.
Synapsin Ia/b CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SYN1 expression without altering the underlying DNA sequence.
Synapsin Ia/b CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SYN1 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 SYN1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Synapsin Ia/b expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SYN1 locus and enabling the study of Synapsin Ia/b-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Synapsin Ia/b pathway restoration in tumor cells with silenced or reduced SYN1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.