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.
Triadin CRISPR Activation Plasmid (m): sc-429407-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Triadin CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Triadin CRISPR Activation Plasmid (m) 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 Triadin CRISPR Activation Plasmid (m) and Triadin CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Trdn 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: Triadin Antibody (IIG12): sc-59724
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Triadin CRISPR Activation Plasmid (m) | sc-429407-ACT | 20 µg | $397.00 | |||
Triadin CRISPR Activation Plasmid (m2) | sc-429407-ACT-2 | 20 µg | $397.00 |
Mouse Trdn encodes triadin, a junctional sarcoplasmic reticulum membrane protein that organizes excitation–contraction coupling in striated muscle by scaffolding the ryanodine receptor (RyR), calsequestrin, and associated luminal partners. Through this calcium-release complex, triadin helps regulate SR Ca²⁺ storage and release kinetics, linking membrane depolarization to Ca²⁺-dependent contraction and downstream calcium-responsive signaling programs. Altered TRDN function perturbs Ca²⁺ homeostasis, destabilizes ryanodine receptor channel behavior, and is associated with muscle and cardiac phenotypes connected to arrhythmogenic and myopathic mechanisms. Trdn is therefore widely studied in pathways governing SR junction architecture, calcium handling, and excitation–contraction coupling fidelity in cardiomyocytes and skeletal muscle fibers.
Triadin CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Trdn expression without altering the underlying DNA sequence.
Triadin CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Trdn 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 Trdn transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Triadin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Trdn locus and enabling the study of Triadin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Triadin pathway restoration in tumor cells with silenced or reduced Trdn expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.