
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MYH9 Lentiviral Activation Particles (m) | sc-421784-LAC | 200 µl | $455.00 |
Myh9 encodes non-muscle myosin IIA (MYH9), an actin-dependent motor protein that generates contractile force and supports cytoskeletal organization in mouse cells. MYH9 regulates adhesion dynamics, cell polarity, and migration by coordinating actomyosin remodeling, stress fiber formation, and mechanotransduction, with downstream effects on processes such as cytokinesis and epithelial barrier integrity. Through interactions with RhoA/ROCK signaling, focal adhesion components, and membrane trafficking machinery, MYH9 helps couple mechanical cues to changes in cell shape and gene expression programs. Altered MYH9 activity has been linked to defects in hematopoietic and renal biology and is widely studied in contexts involving thrombocytopenia, glomerular dysfunction, and cytoskeleton-associated developmental phenotypes.
MYH9 Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Myh9 upregulation across a broader range of human cell types.
MYH9 Lentiviral Activation Particles (m) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the Myh9 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MYH9 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Myh9 genomic locus and regulatory architecture.
The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.