Cacna2d1 CRISPR Activation Plasmid (h): sc-402833-ACT

CACNA2D1 encodes the α2δ1 auxiliary subunit of voltage-gated calcium channels, a key regulator of channel trafficking, membrane localization, and gating properties that shape Ca2+ influx during electrical activity. By tuning calcium-dependent signaling, Cacna2d1 influences excitation–contraction coupling, neurotransmitter release, and downstream pathways linked to transcriptional regulation and cellular stress responses. Altered CACNA2D1 expression has been associated with dysregulated calcium homeostasis in cardiac and neuromuscular contexts and has been studied in relation to arrhythmogenic phenotypes, pain signaling circuitry, and neuronal excitability. As a cell-surface channel complex component, it provides a tractable entry point for dissecting stimulus-dependent calcium signaling and network-level electrophysiological behavior in human model systems.

Cacna2d1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CACNA2D1 expression without altering the underlying DNA sequence.

Cacna2d1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CACNA2D1 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 CACNA2D1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Cacna2d1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CACNA2D1 locus and enabling the study of Cacna2d1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Cacna2d1 pathway restoration in tumor cells with silenced or reduced CACNA2D1 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.