
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
calsequestrin 2 CRISPR Activation Plasmid (h) | sc-402912-ACT | 20 µg | $397.00 | |||
calsequestrin 2 CRISPR Activation Plasmid (h2) | sc-402912-ACT-2 | 20 µg | $397.00 |
CASQ2 encodes calsequestrin 2, the major Ca2+-binding protein in the sarcoplasmic reticulum lumen of cardiomyocytes that buffers intraluminal calcium and helps shape excitation–contraction coupling. By organizing Ca2+ storage and release in proximity to ryanodine receptor complexes, calsequestrin 2 influences calcium-induced calcium release, SR refilling, and calcium homeostasis signaling. Perturbation of CASQ2 expression or function alters SR Ca2+ load and release dynamics, contributing to abnormal calcium handling and arrhythmogenic cellular phenotypes. These properties make CASQ2 a key node for studying cardiac calcium cycling, stress responses, and mechanisms linking SR calcium dysregulation to inherited rhythm disorders.
calsequestrin 2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CASQ2 expression without altering the underlying DNA sequence.
calsequestrin 2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CASQ2 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 CASQ2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous calsequestrin 2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CASQ2 locus and enabling the study of calsequestrin 2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of calsequestrin 2 pathway restoration in tumor cells with silenced or reduced CASQ2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.