Integrin αV/ITGAV/CD51 CRISPR Activation Plasmid (h): sc-400506-ACT

ITGAV encodes integrin αV (CD51), an α subunit that heterodimerizes with multiple β partners (e.g., β3, β5, β6, β8) to form receptors for extracellular matrix ligands containing RGD motifs such as vitronectin, fibronectin, and osteopontin. Through ligand binding and integrin clustering, αV-containing integrins coordinate focal adhesion assembly and mechanotransduction, activating FAK/SRC signaling and downstream PI3K–AKT and MAPK pathways that regulate adhesion, migration, survival, and cytoskeletal remodeling. ITGAV also interfaces with TGF-β biology via αVβ6/αVβ8-mediated activation of latent TGF-β, linking matrix sensing to inflammatory and fibrotic programs. Dysregulated ITGAV activity has been associated with invasive cell behavior, angiogenic responses, and remodeling phenotypes relevant to cancer progression, fibrosis, and immune-microenvironment interactions.

Integrin αV/ITGAV/CD51 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ITGAV expression without altering the underlying DNA sequence.

Integrin αV/ITGAV/CD51 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ITGAV locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the ITGAV transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Integrin αV/ITGAV/CD51 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ITGAV locus and enabling the study of Integrin αV/ITGAV/CD51-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Integrin αV/ITGAV/CD51 pathway restoration in tumor cells with silenced or reduced ITGAV expression.

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