
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MYL10 CRISPR Activation Plasmid (h) | sc-413972-ACT | 20 µg | $397.00 |
MYL10 encodes myosin light chain 10, a regulatory component of the actomyosin cytoskeleton that modulates myosin motor activity and contributes to force generation. Through phosphorylation-dependent control of myosin II function, MYL10 participates in cytoskeletal remodeling processes that influence cell shape, contractility, adhesion, and motility. These mechanisms intersect with pathways governing actin dynamics and Rho/ROCK-dependent contractile signaling, making MYL10 relevant to studies of tissue organization and mechanically regulated cellular behaviors. Altered regulation of cytoskeletal contractility is frequently associated with aberrant migration and invasive phenotypes, supporting investigation of MYL10 in disease-relevant models where actomyosin tension is dysregulated.
MYL10 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MYL10 expression without altering the underlying DNA sequence.
MYL10 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MYL10 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 MYL10 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MYL10 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MYL10 locus and enabling the study of MYL10-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MYL10 pathway restoration in tumor cells with silenced or reduced MYL10 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.