Myosin XVIIIB CRISPR Activation Plasmid (h): sc-410206-ACT

Human MYO18B encodes myosin XVIIIB, an unconventional actin-associated motor protein implicated in organizing cytoskeletal architecture and coordinating actin-dependent processes such as cell adhesion, migration, and intracellular organization. Through interactions with actin networks and scaffolding complexes, MYO18B contributes to mechanotransduction and maintenance of cellular morphology, linking cytoskeletal dynamics to broader signaling programs that regulate tissue structure. Altered MYO18B expression or disruption of cytoskeletal regulation has been reported in studies of tumor biology and muscle-related phenotypes, where changes in actomyosin organization can influence invasion, contractility, and differentiation. As a result, MYO18B is frequently investigated in pathways governing cell motility, cytoskeletal remodeling, and cancer-associated changes in cellular behavior.

Myosin XVIIIB CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MYO18B expression without altering the underlying DNA sequence.

Myosin XVIIIB CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MYO18B 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 MYO18B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Myosin XVIIIB expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MYO18B locus and enabling the study of Myosin XVIIIB-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Myosin XVIIIB pathway restoration in tumor cells with silenced or reduced MYO18B expression.

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