
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
IDS CRISPR Activation Plasmid (h) | sc-404268-ACT | 20 µg | $397.00 |
Human IDS encodes iduronate 2-sulfatase, a lysosomal sulfatase that catalyzes stepwise degradation of the glycosaminoglycans heparan sulfate and dermatan sulfate. By supporting lysosomal catabolic flux, IDS contributes to cellular clearance pathways, endolysosomal homeostasis, and turnover of sulfated extracellular matrix components internalized by endocytosis. Reduced IDS activity disrupts glycosaminoglycan processing and is associated with mucopolysaccharidosis type II (Hunter syndrome), linking IDS function to broader consequences of lysosomal storage on inflammation, proteostasis, and cell signaling.
IDS CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IDS expression without altering the underlying DNA sequence.
IDS CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IDS 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 IDS transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous IDS expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IDS locus and enabling the study of IDS-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of IDS pathway restoration in tumor cells with silenced or reduced IDS expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.