STOX1 CRISPR Activation Plasmid (h): sc-407515-ACT

STOX1 (storkhead box 1) encodes a winged-helix transcription factor that binds DNA and modulates gene programs controlling cell fate decisions, differentiation, and stress-responsive transcription. In human tissues, STOX1 has been implicated in the regulation of trophoblast function and placental development, with reported links to altered transcriptional networks involved in invasion, oxidative stress handling, and inflammatory signaling. Dysregulated STOX1 expression has been associated with pregnancy-related disorders including preeclampsia, and it is also studied for potential roles in neurodevelopmental and neurodegenerative pathways through effects on neuronal gene expression. As a transcriptional regulator, STOX1 provides a useful entry point for dissecting upstream regulatory circuitry and downstream target genes across cell models.

STOX1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous STOX1 expression without altering the underlying DNA sequence.

STOX1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the STOX1 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 STOX1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous STOX1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native STOX1 locus and enabling the study of STOX1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of STOX1 pathway restoration in tumor cells with silenced or reduced STOX1 expression.

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