
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
gp91phox CRISPR Activation Plasmid (m) | sc-419890-ACT | 20 µg | $397.00 |
Cybb encodes gp91phox (NOX2), the catalytic membrane subunit of the phagocyte NADPH oxidase complex that drives reactive oxygen species generation during the respiratory burst. In mouse innate immune cells, gp91phox partners with p22phox and cytosolic regulators such as p47phox, p67phox, and Rac to assemble an electron transport system that reduces oxygen to superoxide, supporting microbial killing and redox-dependent signaling. This activity influences inflammatory pathways, phagolysosomal function, and oxidative stress responses. Disruption or dysregulation of Cybb/NOX2 is widely studied in models of immunodeficiency, chronic inflammation, and redox-linked tissue injury.
gp91phox CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Cybb expression without altering the underlying DNA sequence.
gp91phox CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Cybb 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 Cybb transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous gp91phox expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Cybb locus and enabling the study of gp91phox-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of gp91phox pathway restoration in tumor cells with silenced or reduced Cybb expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.