Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
KCNQ2 CRISPR Activation Plasmid (h): sc-402492-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KCNQ2 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- KCNQ2 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by KCNQ2 CRISPR Activation Plasmid (h) and KCNQ2 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the KCNQ2 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: KCNQ2 Antibody (C-4): sc-271852
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KCNQ2 CRISPR Activation Plasmid (h) | sc-402492-ACT | 20 µg | $397.00 | |||
KCNQ2 CRISPR Activation Plasmid (h2) | sc-402492-ACT-2 | 20 µg | $397.00 |
KCNQ2 encodes the voltage-gated potassium channel subunit Kv7.2, a core component of neuronal M-type K+ currents that stabilize membrane potential and limit repetitive firing. By shaping action potential threshold and spike-frequency adaptation, KCNQ2 influences excitability in cortical and hippocampal circuits and integrates with signaling that modulates channel gating and trafficking, including phosphoinositide-dependent regulation at the plasma membrane. Disruption of KCNQ2 function or expression is strongly linked to epilepsy spectrum disorders and neurodevelopmental phenotypes, making it a widely used locus for studying ion channel biology, synaptic network dynamics, and genotype–phenotype relationships in human neuronal models.
KCNQ2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KCNQ2 expression without altering the underlying DNA sequence.
KCNQ2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KCNQ2 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 KCNQ2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous KCNQ2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KCNQ2 locus and enabling the study of KCNQ2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of KCNQ2 pathway restoration in tumor cells with silenced or reduced KCNQ2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.