
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MYH6 CRISPR Activation Plasmid (h) | sc-400351-ACT | 20 µg | $397.00 |
MYH6 encodes the cardiac alpha-myosin heavy chain, a core component of the myosin II thick filament that powers sarcomere shortening through ATP-dependent actin–myosin cross-bridge cycling. In human myocardium, MYH6 contributes to contractile kinetics, force generation, and coordinated excitation–contraction coupling through interactions with regulatory and structural sarcomeric proteins. MYH6 expression and isoform balance are tightly regulated during development and in response to hemodynamic stress, linking it to pathways governing myofibrillogenesis and cardiac remodeling. Genetic variation or dysregulation of MYH6 has been associated with inherited cardiomyopathies and congenital cardiac phenotypes, making it a frequent target in mechanistic studies of cardiac function.
MYH6 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MYH6 expression without altering the underlying DNA sequence.
MYH6 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MYH6 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 MYH6 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MYH6 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MYH6 locus and enabling the study of MYH6-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MYH6 pathway restoration in tumor cells with silenced or reduced MYH6 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.