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.
T-type Ca++ CP α1H CRISPR Activation Plasmid (h): sc-401147-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- T-type Ca++ CP α1H CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- T-type Ca++ CP α1H 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 T-type Ca++ CP α1H CRISPR Activation Plasmid (h) and T-type Ca++ CP α1H CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the CACNA1H 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: T-type Ca++ CP α1H Antibody (G-10): sc-377510
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
T-type Ca++ CP α1H CRISPR Activation Plasmid (h) | sc-401147-ACT | 20 µg | $397.00 |
CACNA1H encodes the α1H pore-forming subunit of the CaV3.2 T-type voltage-gated calcium channel, which mediates low-voltage–activated Ca2+ influx that shapes subthreshold excitability, rhythmic burst firing, and intracellular calcium-dependent signaling. By coupling membrane depolarization to Ca2+-regulated pathways, CaV3.2 influences neurotransmitter release, hormone secretion, and calcium-dependent transcriptional programs across excitable and non-excitable tissues. Aberrant CACNA1H expression or channel activity has been implicated in disorders involving altered electrical signaling and calcium homeostasis, including epilepsy spectrum phenotypes, pain sensitization, and cardiac rhythm disturbances. As a node in calcium signaling networks, CACNA1H is frequently studied for its contributions to excitability, Ca2+-dependent gene regulation, and stimulus–response coupling.
T-type Ca++ CP α1H CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CACNA1H expression without altering the underlying DNA sequence.
T-type Ca++ CP α1H CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CACNA1H 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 CACNA1H transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous T-type Ca++ CP α1H expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CACNA1H locus and enabling the study of T-type Ca++ CP α1H-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of T-type Ca++ CP α1H pathway restoration in tumor cells with silenced or reduced CACNA1H expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.