OSMR β Lentiviral Activation Particles (h): sc-402700-LAC

OSMR β (oncostatin M receptor beta) is a transmembrane cytokine receptor subunit that forms signaling complexes with gp130 to mediate responses to the IL-6 family cytokine oncostatin M. Ligand engagement activates JAK/STAT, MAPK/ERK, and PI3K/AKT pathways, influencing epithelial and stromal cell differentiation, inflammatory transcriptional programs, and tissue remodeling. OSMR β–dependent signaling is frequently studied in contexts of chronic inflammation and fibrosis, as well as tumor–microenvironment interactions that regulate invasion and extracellular matrix dynamics. As a cell-surface receptor with pathway-specific outputs, OSMR is commonly used to interrogate cytokine-driven transcriptional networks and cross-talk with growth factor signaling.

OSMR β 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 OSMR upregulation across a broader range of human cell types.

OSMR β 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 OSMR transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous OSMR β expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native OSMR 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.