
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Myo-inositol oxygenase CRISPR Activation Plasmid (h) | sc-403646-ACT | 20 µg | $397.00 |
Human MIOX encodes myo-inositol oxygenase, a non-heme diiron enzyme that catalyzes the first committed step of myo-inositol catabolism by converting myo-inositol to D-glucuronic acid. This activity links inositol metabolism to the glucuronate/xylulose pathway and broader carbohydrate handling, influencing cellular redox balance and metabolic flux. MIOX expression is enriched in renal proximal tubule cells and is frequently studied in the context of kidney physiology, metabolic stress responses, and signaling pathways dependent on inositol availability. Dysregulated MIOX activity and transcriptional control have been associated with mechanisms relevant to diabetic kidney injury models and oxidative stress–related phenotypes in renal cells.
Myo-inositol oxygenase CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MIOX expression without altering the underlying DNA sequence.
Myo-inositol oxygenase CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MIOX 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 MIOX transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Myo-inositol oxygenase expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MIOX locus and enabling the study of Myo-inositol oxygenase-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Myo-inositol oxygenase pathway restoration in tumor cells with silenced or reduced MIOX expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.