ZIP7 CRISPR Activation Plasmid (h): sc-409465-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ZIP7 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- ZIP7 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 ZIP7 CRISPR Activation Plasmid (h) and ZIP7 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SLC39A7 transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ZIP7 CRISPR Activation Plasmid (h) | sc-409465-ACT | 20 µg | $397.00 |
SLC39A7 encodes ZIP7, an endoplasmic reticulum and Golgi-localized zinc transporter that regulates cytosolic Zn2+ release to maintain metal ion homeostasis. By controlling zinc-dependent enzyme activity and signaling, ZIP7 influences processes including protein folding in the secretory pathway, ER stress responses, and phosphorylation cascades linked to proliferation and survival. Perturbation of ZIP7-mediated zinc flux has been associated with altered growth factor signaling and dysregulated cellular stress adaptation in multiple disease contexts, including cancer-related pathways. As a central node in zinc signaling, ZIP7 is frequently studied for its impact on transcriptional programs, proteostasis, and metabolic reprogramming.
ZIP7 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLC39A7 expression without altering the underlying DNA sequence.
ZIP7 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLC39A7 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 SLC39A7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ZIP7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLC39A7 locus and enabling the study of ZIP7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ZIP7 pathway restoration in tumor cells with silenced or reduced SLC39A7 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.