
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
INDOL1 CRISPR Activation Plasmid (h) | sc-403856-ACT | 20 µg | $397.00 |
Human IDO2 (indoleamine 2,3-dioxygenase 2; INDOL1) is a heme-dependent enzyme in tryptophan catabolism that contributes to kynurenine pathway flux and local control of amino acid availability. By modulating tryptophan depletion and downstream kynurenine metabolites, IDO2 can influence cellular stress responses, redox balance, and immune-regulatory signaling programs. IDO2 activity intersects with pathways shaping antigen presentation, inflammatory mediator production, and metabolic adaptation, making it relevant to studies of immune evasion, chronic inflammation, and tumor-associated immunometabolism. Dysregulated kynurenine pathway enzymes, including IDO2, have been associated with altered immune tone and metabolic phenotypes observed across cancer and inflammatory disease contexts.
INDOL1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous IDO2 expression without altering the underlying DNA sequence.
INDOL1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the IDO2 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 IDO2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous INDOL1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native IDO2 locus and enabling the study of INDOL1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of INDOL1 pathway restoration in tumor cells with silenced or reduced IDO2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.