
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ADHγ CRISPR Activation Plasmid (h) | sc-402261-ACT | 20 µg | $397.00 |
ADH1C encodes the human alcohol dehydrogenase gamma subunit (ADHγ), a cytosolic, zinc-dependent oxidoreductase that catalyzes the NAD⁺-dependent conversion of ethanol and other short-chain alcohols to their corresponding aldehydes. This enzyme contributes to hepatic and gastrointestinal alcohol metabolism and interfaces with retinoid and lipid-derived aldehyde handling through alcohol/aldehyde interconversion and redox balance. Variation in ADH1C expression or activity can modulate acetaldehyde generation and oxidative stress, influencing susceptibility to alcohol-related tissue injury and broader metabolic phenotypes. As a result, ADHγ is frequently studied in pathways linking xenobiotic metabolism, cellular redox homeostasis, and inflammatory signaling.
ADHγ CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ADH1C expression without altering the underlying DNA sequence.
ADHγ CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ADH1C 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 ADH1C transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ADHγ expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ADH1C locus and enabling the study of ADHγ-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ADHγ pathway restoration in tumor cells with silenced or reduced ADH1C expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.