T-type Ca++ CP α1I CRISPR Activation Plasmid (h): sc-403786-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- T-type Ca++ CP α1I CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- T-type Ca++ CP α1I 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 α1I CRISPR Activation Plasmid (h) and T-type Ca++ CP α1I CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the CACNA1I 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 α1I Antibody (3H5): sc-293486
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
T-type Ca++ CP α1I CRISPR Activation Plasmid (h) | sc-403786-ACT | 20 µg | $397.00 |
CACNA1I encodes the CaV3.3 T-type calcium channel α1I subunit, a low-voltage–activated pore-forming protein that mediates transient Ca2+ influx near resting membrane potentials. By shaping subthreshold depolarizations and rebound bursting, CaV3.3 contributes to neuronal excitability, rhythmic firing, and Ca2+-dependent signaling that couples membrane activity to transcriptional and synaptic plasticity programs. CACNA1I activity intersects with pathways controlling membrane potential dynamics, intracellular calcium homeostasis, and activity-dependent gene regulation in excitable tissues. Genetic and functional studies have implicated CACNA1I variation or dysregulation in neuropsychiatric and neurodevelopmental phenotypes, supporting its relevance for mechanistic work on circuit-level oscillations and cellular excitability.
T-type Ca++ CP α1I CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CACNA1I expression without altering the underlying DNA sequence.
T-type Ca++ CP α1I CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CACNA1I 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 CACNA1I transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous T-type Ca++ CP α1I expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CACNA1I locus and enabling the study of T-type Ca++ CP α1I-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 α1I pathway restoration in tumor cells with silenced or reduced CACNA1I expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.