TDO2 CRISPR Activation Plasmid (m): sc-425274-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TDO2 CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- TDO2 CRISPR Activation Plasmid (m) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by TDO2 CRISPR Activation Plasmid (m) and TDO2 CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Tdo2 transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TDO2 CRISPR Activation Plasmid (m) | sc-425274-ACT | 20 µg | $397.00 |
Mouse Tdo2 encodes tryptophan 2,3-dioxygenase (TDO2), a heme-dependent enzyme that catalyzes the first and rate-limiting step of tryptophan catabolism through the kynurenine pathway. By controlling conversion of L-tryptophan to N-formylkynurenine, TDO2 influences cellular tryptophan availability, downstream NAD⁺-related metabolite production, and aryl hydrocarbon receptor–linked immunometabolic signaling via kynurenine. Tdo2 activity is tightly connected to hepatic metabolic homeostasis and systemic amino acid balance, with downstream effects on oxidative stress responses and inflammatory programs. Dysregulated kynurenine pathway flux has been associated with immune modulation and neuroinflammatory phenotypes, making Tdo2 a relevant target for mechanistic studies of metabolism–immunity crosstalk in mouse models.
TDO2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Tdo2 expression without altering the underlying DNA sequence.
TDO2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Tdo2 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 Tdo2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TDO2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Tdo2 locus and enabling the study of TDO2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TDO2 pathway restoration in tumor cells with silenced or reduced Tdo2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.