Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
DDIT3/CHOP/GADD153 CRISPR Activation Plasmid (m): sc-419970-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DDIT3/GADD153/CHOP CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- DDIT3/GADD153/CHOP 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 DDIT3/GADD153/CHOP CRISPR Activation Plasmid (m) and DDIT3/GADD153/CHOP CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Ddit3 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: DDIT3/GADD153/CHOP Antibody (B-3): sc-7351
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DDIT3/CHOP/GADD153 CRISPR Activation Plasmid (m) | sc-419970-ACT | 20 µg | $397.00 |
Ddit3 encodes the stress-inducible transcription factor DDIT3/CHOP/GADD153, a central effector of the integrated stress response and endoplasmic reticulum (ER) stress–driven unfolded protein response. CHOP heterodimerizes with C/EBP family members to remodel gene expression programs that influence apoptosis, autophagy, redox balance, and cell-cycle control during proteotoxic and metabolic stress. In mouse cells, Ddit3 is commonly used as a molecular readout of ER stress downstream of PERK–eIF2α–ATF4 signaling and intersects with mitochondrial dysfunction and inflammatory pathways. Dysregulated Ddit3 activity has been implicated in models of metabolic disease, neurodegeneration, tissue injury, and tumor biology, supporting its use in mechanistic studies of stress adaptation and cell fate decisions.
DDIT3/GADD153/CHOP CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Ddit3 expression without altering the underlying DNA sequence.
DDIT3/GADD153/CHOP CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Ddit3 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 Ddit3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DDIT3/GADD153/CHOP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Ddit3 locus and enabling the study of DDIT3/GADD153/CHOP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DDIT3/GADD153/CHOP pathway restoration in tumor cells with silenced or reduced Ddit3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.