VCAM-1 Lentiviral Activation Particles (h): sc-400135-LAC

VCAM1 encodes vascular cell adhesion molecule 1 (VCAM-1/CD106), an inducible immunoglobulin superfamily receptor expressed on activated endothelial cells that mediates firm leukocyte adhesion and transmigration through binding to integrins such as VLA-4 (ITGA4/ITGB1). Its expression is strongly upregulated by inflammatory cues through NF-κB- and cytokine-driven programs, linking vascular activation to immune cell recruitment, endothelial barrier remodeling, and extracellular matrix interactions. VCAM-1 participates in signaling networks that coordinate cytoskeletal dynamics and cell–cell adhesion during inflammatory responses. Dysregulated VCAM1 expression is associated with chronic inflammation and vascular dysfunction, and is frequently studied in contexts such as atherosclerosis, autoimmune pathology, and tumor-associated endothelium.

VCAM-1 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 VCAM1 upregulation across a broader range of human cell types.

VCAM-1 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 VCAM1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous VCAM-1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native VCAM1 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.