
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
USP9X CRISPR Activation Plasmid (h) | sc-402285-ACT | 20 µg | $397.00 |
USP9X (ubiquitin specific peptidase 9 X-linked) is a deubiquitinating enzyme that regulates protein stability and signaling output by removing ubiquitin chains from substrate proteins. It influences proteostasis, endocytic trafficking, and stress-response pathways, and has been linked to modulation of apoptosis, cell-cycle control, and DNA damage responses through context-dependent stabilization of key signaling components. USP9X activity intersects with ubiquitin–proteasome and autophagy networks, shaping cellular differentiation and survival decisions. Dysregulated USP9X expression or function has been associated with multiple cancers and neurodevelopmental phenotypes, making it a relevant target for mechanistic studies of ubiquitin signaling in human cells.
USP9X CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous USP9X expression without altering the underlying DNA sequence.
USP9X CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the USP9X 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 USP9X transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous USP9X expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native USP9X locus and enabling the study of USP9X-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of USP9X pathway restoration in tumor cells with silenced or reduced USP9X expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.