Integrin αV/ITGAV/CD51 Lentiviral Activation Particles (h): sc-400506-LAC

ITGAV encodes integrin αV (CD51), an α subunit that pairs with β integrins (commonly ITGB3, ITGB5, ITGB6, or ITGB8) to form receptors for extracellular matrix ligands such as vitronectin, fibronectin, osteopontin, and latent TGF-β complexes. Through outside-in and inside-out signaling, αV-containing integrins regulate focal adhesion dynamics, actin cytoskeletal remodeling, and mechanotransduction via FAK/SRC, PI3K–AKT, and MAPK pathways. Integrin αV also contributes to cell migration, invasion, survival signaling, and crosstalk with growth factor receptors, shaping tissue remodeling and inflammatory responses. Dysregulated ITGAV activity and αV-integrin signaling are frequently studied in cancer progression, angiogenesis, fibrosis, and bone and immune biology where altered adhesion and TGF-β activation programs are implicated.

Integrin αV/ITGAV/CD51 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 ITGAV upregulation across a broader range of human cell types.

Integrin αV/ITGAV/CD51 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 ITGAV transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Integrin αV/ITGAV/CD51 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native ITGAV 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.