
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SELH CRISPR Activation Plasmid (h) | sc-415276-ACT | 20 µg | $397.00 | |||
SELH CRISPR Activation Plasmid (h2) | sc-415276-ACT-2 | 20 µg | $397.00 |
Human SELENOH encodes selenoprotein H (SELH), a redox-active, nucleus-associated protein implicated in maintaining cellular redox homeostasis through thiol-dependent antioxidant processes. SELH contributes to the cellular response to oxidative stress and supports transcriptional programs that influence DNA integrity, mitochondrial function, and proteostasis under redox challenge. As part of the broader selenoprotein network that couples selenium metabolism to reactive oxygen species control, altered SELH activity is relevant to mechanisms underlying neurodegeneration, metabolic dysfunction, and tumor biology where oxidative signaling and stress adaptation are perturbed.
SELH CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SELENOH expression without altering the underlying DNA sequence.
SELH CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SELENOH 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 SELENOH transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SELH expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SELENOH locus and enabling the study of SELH-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SELH pathway restoration in tumor cells with silenced or reduced SELENOH expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.