NDRG1 CRISPR Activation Plasmid (h): sc-402294-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NDRG1 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- NDRG1 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 NDRG1 CRISPR Activation Plasmid (h) and NDRG1 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the NDRG1 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: NDRG1 Antibody (B-5): sc-398291
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NDRG1 CRISPR Activation Plasmid (h) | sc-402294-ACT | 20 µg | $397.00 | |||
NDRG1 CRISPR Activation Plasmid (h2) | sc-402294-ACT-2 | 20 µg | $397.00 |
NDRG1 (N-myc downstream regulated gene 1) encodes a stress-responsive cytoplasmic protein implicated in cellular differentiation, lipid and iron homeostasis, and modulation of signal transduction networks. NDRG1 is regulated by hypoxia, p53, and oncogenic MYC signaling and has been linked to pathways controlling proliferation, epithelial–mesenchymal dynamics, and responses to cellular stress. In human biology, altered NDRG1 expression has been associated with tumor progression and metastatic behavior in multiple tissue contexts, as well as inherited peripheral neuropathy phenotypes. These features make NDRG1 a useful node for dissecting transcriptional programs that couple microenvironmental stress to changes in cell state.
NDRG1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous NDRG1 expression without altering the underlying DNA sequence.
NDRG1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the NDRG1 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 NDRG1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous NDRG1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native NDRG1 locus and enabling the study of NDRG1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of NDRG1 pathway restoration in tumor cells with silenced or reduced NDRG1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.