Integrin β3/ITGB3/CD61 Lentiviral Activation Particles (m): sc-421175-LAC

Itgb3 encodes integrin β3 (CD61), a transmembrane adhesion receptor that pairs with αIIb or αV to form integrins central to platelet aggregation, cell–matrix interactions, and mechanotransduction. ITGB3-mediated outside-in and inside-out signaling coordinates focal adhesion dynamics and cytoskeletal remodeling through pathways such as FAK/Src, PI3K–AKT, and MAPK, thereby influencing migration, survival, and differentiation. In mouse models, Itgb3 function is widely studied in thrombosis and hemostasis biology, as well as in angiogenesis and tumor-associated stromal interactions, where altered integrin signaling can modulate inflammation and tissue remodeling.

Integrin β3/ITGB3/CD61 Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Itgb3 upregulation across a broader range of human cell types.

Integrin β3/ITGB3/CD61 Lentiviral Activation Particles (m) 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 Itgb3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Integrin β3/ITGB3/CD61 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Itgb3 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.