
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SETX CRISPR Activation Plasmid (h) | sc-402354-ACT | 20 µg | $397.00 |
Human SETX encodes senataxin, a superfamily 1 DNA/RNA helicase that resolves RNA:DNA hybrids (R-loops) and supports transcription termination, replication–transcription conflict resolution, and genome stability maintenance. SETX participates in the DNA damage response, coupling RNA processing with repair of transcription-associated lesions and limiting aberrant recombination at highly transcribed loci. Disruption of SETX function is linked to neurodegenerative and neuromuscular phenotypes, including ataxia with oculomotor apraxia type 2 and juvenile amyotrophic lateral sclerosis, highlighting its relevance to RNA metabolism and stress-response pathways.
SETX CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SETX expression without altering the underlying DNA sequence.
SETX CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SETX 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 SETX transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SETX expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SETX locus and enabling the study of SETX-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SETX pathway restoration in tumor cells with silenced or reduced SETX expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.