KCNQ3 CRISPR Activation Plasmid (h): sc-403544-ACT

KCNQ3 encodes the Kv7.3 voltage-gated potassium channel subunit, a core component of neuronal M-type K⁺ currents that stabilize membrane potential and constrain repetitive firing. By shaping subthreshold excitability and spike-frequency adaptation, KCNQ3 influences synaptic integration and network oscillations, intersecting with cholinergic and phosphoinositide-dependent signaling that modulates channel gating. Altered KCNQ3 expression or function has been linked to neurodevelopmental and epileptic phenotypes, highlighting its relevance to studies of cortical excitability and circuit homeostasis. Human KCNQ3 is therefore widely used in mechanistic research on ion channel regulation, neuronal signaling pathways, and genotype–phenotype relationships in excitability disorders.

KCNQ3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KCNQ3 expression without altering the underlying DNA sequence.

KCNQ3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KCNQ3 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 KCNQ3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous KCNQ3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KCNQ3 locus and enabling the study of KCNQ3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of KCNQ3 pathway restoration in tumor cells with silenced or reduced KCNQ3 expression.

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