STC2 CRISPR Activation Plasmid (h): sc-405292-ACT

Human STC2 (stanniocalcin 2) encodes a secreted glycoprotein hormone implicated in calcium/phosphate homeostasis and cellular adaptation to stress. STC2 expression is regulated by hypoxia and endoplasmic reticulum stress pathways and has been linked to modulation of proliferation, apoptosis, and metabolic remodeling through context-dependent signaling networks. Dysregulated STC2 levels have been reported across multiple disease settings, including cancer biology and cardiometabolic and inflammatory processes, where it is frequently studied as a stress-responsive mediator. These properties make STC2 a useful target for dissecting secreted factor signaling, stress pathway crosstalk, and phenotypes tied to microenvironmental adaptation.

STC2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous STC2 expression without altering the underlying DNA sequence.

STC2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the STC2 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 STC2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous STC2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native STC2 locus and enabling the study of STC2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of STC2 pathway restoration in tumor cells with silenced or reduced STC2 expression.

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