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.
KCNMB4 CRISPR Activation Plasmid (h): sc-405044-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KCNMB4 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- KCNMB4 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 KCNMB4 CRISPR Activation Plasmid (h) and KCNMB4 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the KCNMB4 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: KCNMB4 Antibody (B-6): sc-515712
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KCNMB4 CRISPR Activation Plasmid (h) | sc-405044-ACT | 20 µg | $397.00 |
KCNMB4 encodes the β4 auxiliary subunit of large-conductance, calcium- and voltage-activated potassium (BK) channels, modulating channel gating kinetics, calcium sensitivity, and membrane excitability. In human neurons and other excitable tissues, KCNMB4 helps tune action potential firing and calcium-dependent repolarization, integrating with Ca2+ signaling and electrophysiological homeostasis. By shaping BK channel behavior, it influences processes such as neurotransmission, spike frequency adaptation, and activity-dependent signaling pathways linked to ion-channel regulation. Dysregulated BK channel composition, including altered β-subunit expression, is implicated in neurological phenotypes where excitability balance is disrupted, supporting its utility in mechanistic studies of channelopathies and excitability-driven cellular stress.
KCNMB4 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous KCNMB4 expression without altering the underlying DNA sequence.
KCNMB4 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the KCNMB4 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 KCNMB4 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous KCNMB4 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native KCNMB4 locus and enabling the study of KCNMB4-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of KCNMB4 pathway restoration in tumor cells with silenced or reduced KCNMB4 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.