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.
GGT5 CRISPR Activation Plasmid (h): sc-405055-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GGT5 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- GGT5 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 GGT5 CRISPR Activation Plasmid (h) and GGT5 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the GGT5 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: GGT5 Antibody (F-8): sc-373693
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GGT5 CRISPR Activation Plasmid (h) | sc-405055-ACT | 20 µg | $397.00 |
Human GGT5 encodes gamma-glutamyltransferase 5, a cell-surface enzyme that hydrolyzes the gamma-glutamyl bond of glutathione and related conjugates to support extracellular glutathione turnover and amino acid salvage. Through its role in the gamma-glutamyl cycle, GGT5 contributes to redox homeostasis, cysteine availability, and metabolism of glutathione-derived intermediates, with downstream effects on oxidative stress signaling and cellular detoxification processes. GGT5 activity has been studied in contexts involving inflammatory microenvironments, lipid and xenobiotic metabolism, and tissue-specific regulation of oxidative balance, making it relevant to disease-associated pathways where redox state and glutathione handling are perturbed. These features position GGT5 as a useful node for dissecting how glutathione catabolism influences signaling, metabolic adaptation, and cellular stress responses.
GGT5 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GGT5 expression without altering the underlying DNA sequence.
GGT5 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GGT5 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 GGT5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GGT5 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GGT5 locus and enabling the study of GGT5-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GGT5 pathway restoration in tumor cells with silenced or reduced GGT5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.