Superoxide Dismutase 2/SOD2 CRISPR Activation Plasmid (h): sc-400230-ACT

Human SOD2 encodes the mitochondrial manganese superoxide dismutase that converts superoxide radicals into hydrogen peroxide and oxygen, forming a primary antioxidant defense within the mitochondrial matrix. By limiting oxidative damage to mitochondrial DNA, proteins, and lipids, SOD2 helps preserve respiratory chain function and supports cellular redox homeostasis, stress adaptation, and apoptotic signaling. SOD2 activity integrates with ROS-sensitive pathways including NRF2-mediated antioxidant programs, inflammatory signaling, and mitochondrial quality control processes such as mitophagy. Altered SOD2 expression or function is associated with oxidative stress phenotypes observed across cancer biology, neurodegeneration, cardiometabolic dysfunction, and inflammatory disease models, making it a common target for mechanistic studies of mitochondrial ROS.

Superoxide Dismutase 2/SOD2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SOD2 expression without altering the underlying DNA sequence.

Superoxide Dismutase 2/SOD2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SOD2 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 SOD2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Superoxide Dismutase 2/SOD2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SOD2 locus and enabling the study of Superoxide Dismutase 2/SOD2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Superoxide Dismutase 2/SOD2 pathway restoration in tumor cells with silenced or reduced SOD2 expression.

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