Selenoprotein P CRISPR Activation Plasmid (h): sc-417457-ACT

SELENOP encodes selenoprotein P, a secreted glycoprotein that functions as a major selenium transport factor in plasma and supports systemic selenium distribution to peripheral tissues. Through delivery of selenium for selenoenzyme biosynthesis, SELENOP contributes to cellular redox homeostasis, antioxidant defense, and protection from oxidative and inflammatory stress, with relevance to liver function and metabolic regulation. Altered SELENOP expression has been associated with dysregulated oxidative stress responses and metabolic disease phenotypes, and it is frequently examined in the context of insulin signaling, lipid metabolism, and inflammatory pathways. As a circulating hepatokine-like factor, selenoprotein P is also used as a molecular readout for hepatic secretory programs and nutrient-responsive transcriptional control.

Selenoprotein P CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SELENOP expression without altering the underlying DNA sequence.

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

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