
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MYH9 CRISPR Activation Plasmid (m) | sc-421784-ACT | 20 µg | $397.00 |
Myh9 encodes non-muscle myosin heavy chain IIA (MYH9), a core actin-based motor that generates contractile force and supports cortical tension, adhesion dynamics, and cytokinesis. MYH9 activity integrates with RhoA/ROCK signaling, actin stress fiber remodeling, and focal adhesion turnover to regulate cell polarity, migration, and mechanotransduction. In mouse tissues, Myh9 contributes to hematopoietic and immune cell function, epithelial integrity, and developmental morphogenesis, making it a useful node for studying cytoskeletal control of tissue architecture. Dysregulated MYH9-dependent contractility is linked to defects in cell division and barrier function and is frequently examined in models of inflammation, fibrosis, and cancer-associated invasion.
MYH9 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Myh9 expression without altering the underlying DNA sequence.
MYH9 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Myh9 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 Myh9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MYH9 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Myh9 locus and enabling the study of MYH9-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MYH9 pathway restoration in tumor cells with silenced or reduced Myh9 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.