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.
L-type Ca++ CP α1C CRISPR Activation Plasmid (h): sc-401062-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- L-type Ca++ CP α1C CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- L-type Ca++ CP α1C 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 L-type Ca++ CP α1C CRISPR Activation Plasmid (h) and L-type Ca++ CP α1C CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the CACNA1C 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: L-type Ca++ CP α1C Antibody (D-6): sc-398433
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
L-type Ca++ CP α1C CRISPR Activation Plasmid (h) | sc-401062-ACT | 20 µg | $397.00 | |||
L-type Ca++ CP α1C CRISPR Activation Plasmid (h2) | sc-401062-ACT-2 | 20 µg | $397.00 |
CACNA1C encodes the α1C pore-forming subunit of the CaV1.2 L-type Ca2+ channel, a principal mediator of voltage-dependent calcium influx in excitable and non-excitable human cells. Channel opening couples membrane depolarization to intracellular Ca2+ signaling, shaping excitation–contraction coupling, pacemaker activity, and activity-dependent transcription through pathways such as CaM/CaMK and calcineurin–NFAT. CaV1.2-dependent calcium entry also regulates neurotransmitter release dynamics and synaptic plasticity via calcium-sensitive effectors and downstream gene expression programs. Genetic variation or dysregulated CACNA1C expression has been linked to altered electrophysiology and calcium homeostasis in cardiovascular and neuropsychiatric disease contexts, supporting its use in mechanistic studies of signaling and cellular excitability.
L-type Ca++ CP α1C CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CACNA1C expression without altering the underlying DNA sequence.
L-type Ca++ CP α1C CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CACNA1C 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 CACNA1C transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous L-type Ca++ CP α1C expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CACNA1C locus and enabling the study of L-type Ca++ CP α1C-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of L-type Ca++ CP α1C pathway restoration in tumor cells with silenced or reduced CACNA1C expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.