STC2 Lentiviral Activation Particles (h): sc-405292-LAC

STC2 (stanniocalcin 2) is a secreted glycoprotein hormone-like factor implicated in cellular adaptation to metabolic and environmental stress. In human cells, STC2 is induced by endoplasmic reticulum stress and nutrient signaling and can modulate calcium and phosphate homeostasis, oxidative stress responses, and survival pathways, including crosstalk with PI3K–AKT and hypoxia-associated programs. Altered STC2 expression has been reported across multiple tumor types and is frequently studied in relation to proliferation, invasion, angiogenic signaling, and therapy response phenotypes. Beyond oncology, STC2 is relevant to research on inflammation, fibrosis, and tissue remodeling where secreted stress-response mediators shape paracrine signaling.

STC2 Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient STC2 upregulation across a broader range of human cell types.

STC2 Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the STC2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous STC2 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native STC2 genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

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