
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GlyR α3 CRISPR Activation Plasmid (h) | sc-403621-ACT | 20 µg | $397.00 |
GLRA3 encodes the glycine receptor α3 (GlyR α3), a ligand-gated chloride channel subunit that mediates fast inhibitory neurotransmission in the central nervous system. Upon glycine binding, GlyR α3 contributes to chloride influx, membrane hyperpolarization, and regulation of neuronal excitability within synaptic signaling circuits. GLRA3 function intersects with inhibitory neurotransmitter receptor activity, ion transmembrane transport, and synaptic plasticity processes that shape sensory processing and network stability. Altered GlyR α3 expression or signaling has been associated with neurological phenotypes linked to disrupted inhibitory tone, including pain-related sensitization and seizure susceptibility in experimental contexts.
GlyR α3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GLRA3 expression without altering the underlying DNA sequence.
GlyR α3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GLRA3 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 GLRA3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GlyR α3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GLRA3 locus and enabling the study of GlyR α3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GlyR α3 pathway restoration in tumor cells with silenced or reduced GLRA3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.