
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Espin CRISPR Activation Plasmid (h) | sc-403106-ACT | 20 µg | $397.00 |
Human ESPN encodes espin, an actin-bundling protein that regulates the assembly and stability of parallel actin filament bundles in microvilli and stereocilia. Espin supports specialized protrusion morphogenesis, mechanosensory architecture, and cytoskeletal remodeling by coordinating actin dynamics and membrane-associated scaffolding. Through its impact on stereocilia organization, ESPN is linked to sensory hair cell function and is studied in pathways governing epithelial surface specialization and mechanotransduction. Dysregulation or genetic alteration of ESPN has been associated with inherited hearing impairment and related defects in stereocilia structure, making it relevant for investigating cytoskeletal disease mechanisms.
Espin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ESPN expression without altering the underlying DNA sequence.
Espin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ESPN 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 ESPN transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Espin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ESPN locus and enabling the study of Espin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Espin pathway restoration in tumor cells with silenced or reduced ESPN expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.