
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Myosin Id CRISPR Activation Plasmid (h) | sc-403425-ACT | 20 µg | $397.00 |
Human MYO1D encodes myosin Id, an actin-based, membrane-associated motor implicated in coupling the cortical actin cytoskeleton to intracellular membranes. Myosin Id supports processes such as membrane trafficking, endocytic recycling, and organization of cell polarity and shape, linking cytoskeletal remodeling to spatial control of signaling at the plasma membrane. Through these functions, MYO1D can influence pathways that depend on directed vesicle transport and cytoskeleton-dependent receptor distribution. Dysregulation of actin–membrane dynamics and polarity programs is relevant to disease-associated phenotypes including altered cell migration and epithelial organization, making MYO1D a useful target for mechanistic studies in cellular homeostasis.
Myosin Id CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MYO1D expression without altering the underlying DNA sequence.
Myosin Id CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MYO1D 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 MYO1D transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Myosin Id expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MYO1D locus and enabling the study of Myosin Id-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Myosin Id pathway restoration in tumor cells with silenced or reduced MYO1D expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.