
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Myosin If CRISPR Activation Plasmid (h) | sc-403977-ACT | 20 µg | $397.00 |
MYO1F encodes Myosin If, an actin-dependent motor protein enriched in hematopoietic cells that supports membrane dynamics, cortical actin remodeling, and force generation during adhesion and migration. Myosin If contributes to vesicle trafficking, phagocytic cup formation, and integrin-associated cytoskeletal organization, linking ATP-driven motility to immune cell polarity and signaling. Altered MYO1F expression or function has been associated with dysregulated leukocyte motility and inflammatory responses, making it relevant to studies of immune homeostasis and immune-mediated disease mechanisms. Its activity interfaces with actin regulatory pathways that coordinate endocytosis, chemotaxis, and immune synapse architecture.
Myosin If CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MYO1F expression without altering the underlying DNA sequence.
Myosin If CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MYO1F 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 MYO1F transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Myosin If expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MYO1F locus and enabling the study of Myosin If-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Myosin If pathway restoration in tumor cells with silenced or reduced MYO1F expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.