
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
T-type Ca++ CP α1G CRISPR Activation Plasmid (h) | sc-418331-ACT | 20 µg | $397.00 | |||
T-type Ca++ CP α1G CRISPR Activation Plasmid (h2) | sc-418331-ACT-2 | 20 µg | $397.00 |
CACNA1G encodes the α1G pore-forming subunit of the Cav3.1 T-type Ca++ channel, a low-voltage–activated conductance that supports window currents and rhythmic membrane depolarization. By shaping intracellular calcium transients near resting potentials, Cav3.1 influences neuronal excitability, pacemaking, and calcium-dependent signaling cascades that couple membrane activity to gene regulation and synaptic function. CACNA1G activity integrates with broader Ca2+ homeostasis networks and excitability pathways, including calcium-dependent kinases and transcriptional programs responsive to membrane potential. Dysregulated T-type calcium channel function has been associated in the literature with altered thalamocortical oscillations and excitability phenotypes relevant to neurological and neuropsychiatric disease mechanisms.
T-type Ca++ CP α1G CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CACNA1G expression without altering the underlying DNA sequence.
T-type Ca++ CP α1G CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CACNA1G 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 CACNA1G transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous T-type Ca++ CP α1G expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CACNA1G locus and enabling the study of T-type Ca++ CP α1G-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 α1G pathway restoration in tumor cells with silenced or reduced CACNA1G expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.