
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FHOD3 CRISPR Activation Plasmid (h) | sc-405102-ACT | 20 µg | $397.00 |
FHOD3 (formin homology 2 domain containing 3) encodes an actin-nucleating formin that coordinates filament elongation and organization of the cytoskeleton. In striated muscle, FHOD3 supports sarcomere integrity and myofibrillogenesis, linking Rho family GTPase signaling to actin remodeling and contractile apparatus maintenance. Altered FHOD3 expression or variation has been associated with cardiomyocyte structural defects and is studied in the context of cardiomyopathies and broader cytoskeletal dysregulation. As a regulator of actin dynamics, FHOD3 is relevant to investigations of cell morphology, mechanotransduction, and muscle cell maturation.
FHOD3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FHOD3 expression without altering the underlying DNA sequence.
FHOD3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FHOD3 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 FHOD3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FHOD3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FHOD3 locus and enabling the study of FHOD3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FHOD3 pathway restoration in tumor cells with silenced or reduced FHOD3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.