Superoxide Dismutase 1/SOD1 CRISPR Activation Plasmid (m): sc-423069-ACT

Mouse Sod1 encodes superoxide dismutase 1 (SOD1), a predominantly cytosolic Cu/Zn metalloenzyme that catalyzes dismutation of superoxide anion into hydrogen peroxide and oxygen, thereby limiting oxidative damage to proteins, lipids, and nucleic acids. By shaping cellular redox homeostasis, SOD1 influences mitochondrial function, antioxidant network balance (e.g., peroxiredoxin and catalase-dependent peroxide handling), and stress-responsive signaling pathways including MAPK and NF-κB. Perturbation of SOD1 activity alters reactive oxygen species flux and can impact proteostasis, neuroinflammation, and cell survival under oxidative stress. SOD1 biology is widely studied in the context of redox dysregulation and models of neurodegeneration, as well as broader oxidative stress–associated phenotypes in metabolism and aging.

Superoxide Dismutase 1/SOD1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Sod1 expression without altering the underlying DNA sequence.

Superoxide Dismutase 1/SOD1 CRISPR Activation Plasmid (m) 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.