
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KCNQ5 CRISPR Activation Plasmid (h) | sc-403289-ACT | 20 µg | $397.00 |
KCNQ5 encodes the voltage-gated potassium channel subunit Kv7.5, a member of the KCNQ/Kv7 family that contributes to membrane repolarization and control of cellular excitability. By conducting M-type potassium currents, KCNQ5 helps regulate resting membrane potential and firing properties in excitable cells, integrating with ion transport and calcium-dependent signaling processes. Altered KCNQ channel activity is broadly relevant to neurophysiology and sensory signaling, and dysregulation of potassium conductance has been associated with disorders involving aberrant neuronal excitability and network activity. In research settings, KCNQ5 modulation is used to interrogate channel biology, electrophysiological phenotypes, and pathway-level effects of altered potassium flux.
KCNQ5 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KCNQ5 expression without altering the underlying DNA sequence.
KCNQ5 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KCNQ5 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 KCNQ5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous KCNQ5 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KCNQ5 locus and enabling the study of KCNQ5-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of KCNQ5 pathway restoration in tumor cells with silenced or reduced KCNQ5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.