Superoxide Dismutase 1/SOD1 CRISPR Activation Plasmid (h): sc-400186-ACT

SOD1 encodes the cytosolic Cu/Zn superoxide dismutase that catalyzes dismutation of superoxide anions into hydrogen peroxide and oxygen, forming a primary enzymatic barrier against reactive oxygen species. By shaping redox homeostasis, SOD1 influences oxidative stress responses, mitochondrial function, and downstream signaling pathways that regulate inflammation, proteostasis, and apoptosis. Altered SOD1 activity perturbs cellular antioxidant capacity and can contribute to protein misfolding and motor neuron vulnerability, with strong relevance to neurodegeneration and broader stress-associated phenotypes. Human SOD1 is therefore widely studied in models of redox imbalance, aggregation biology, and oxidative damage–linked cellular dysfunction.

Superoxide Dismutase 1/SOD1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SOD1 expression without altering the underlying DNA sequence.

Superoxide Dismutase 1/SOD1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SOD1 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 SOD1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Superoxide Dismutase 1/SOD1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SOD1 locus and enabling the study of Superoxide Dismutase 1/SOD1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Superoxide Dismutase 1/SOD1 pathway restoration in tumor cells with silenced or reduced SOD1 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.