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.
DnaJC3 CRISPR Activation Plasmid (h): sc-405100-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DnaJC3 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- DnaJC3 CRISPR Activation Plasmid (h) 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 DnaJC3 CRISPR Activation Plasmid (h) and DnaJC3 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the DNAJC3 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: DnaJC3 Antibody (A-7): sc-393559
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DnaJC3 CRISPR Activation Plasmid (h) | sc-405100-ACT | 20 µg | $397.00 | |||
DnaJC3 CRISPR Activation Plasmid (h2) | sc-405100-ACT-2 | 20 µg | $397.00 |
DNAJC3 encodes DnaJC3, an endoplasmic reticulum–associated Hsp40 co-chaperone that modulates proteostasis by interacting with BiP/GRP78 and attenuating PERK-mediated signaling during the unfolded protein response. By linking chaperone activity to ER stress sensing, DnaJC3 helps regulate translational control, protein folding capacity, and recovery from proteotoxic stress, with downstream effects on apoptosis and inflammatory signaling. Dysregulation of ER stress pathways involving DnaJC3 has been connected to cellular vulnerability in metabolic and neurodegenerative contexts, where chronic UPR activation can impair secretory function and mitochondrial homeostasis. As a node in ER quality control, DnaJC3 is relevant for mechanistic studies of stress adaptation, proteome remodeling, and cell fate decisions under nutrient or oxidative stress.
DnaJC3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DNAJC3 expression without altering the underlying DNA sequence.
DnaJC3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DNAJC3 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 DNAJC3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DnaJC3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DNAJC3 locus and enabling the study of DnaJC3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DnaJC3 pathway restoration in tumor cells with silenced or reduced DNAJC3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.