SELENBP1 CRISPR Activation Plasmid (m): sc-422870-ACT

Mouse Selenbp1 encodes selenium-binding protein 1 (SELENBP1), a conserved cytosolic protein implicated in cellular selenium handling and redox homeostasis. SELENBP1 expression is frequently linked to metabolic state and differentiation, with reported connections to oxidative stress responses, mitochondrial function, and regulation of reactive sulfur/selenium species. Altered SELENBP1 levels have been associated with changes in cell proliferation and invasiveness in cancer biology, and have also been studied in contexts of inflammation and tissue injury where redox balance is perturbed. As a marker of cellular metabolic and oxidative status, SELENBP1 is useful for dissecting pathways that couple selenium biology to transcriptional programs and stress-adaptation phenotypes.

SELENBP1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Selenbp1 expression without altering the underlying DNA sequence.

SELENBP1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Selenbp1 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 Selenbp1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SELENBP1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Selenbp1 locus and enabling the study of SELENBP1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SELENBP1 pathway restoration in tumor cells with silenced or reduced Selenbp1 expression.

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