Integrin α3/ITGA3/CD49c CRISPR Activation Plasmid (h): sc-400841-ACT

ITGA3 encodes integrin α3 (CD49c), an α subunit that forms the α3β1 heterodimer to mediate cell–extracellular matrix adhesion, particularly to laminins within basement membranes. Through coupling to focal adhesion complexes, ITGA3 regulates cytoskeletal remodeling, cell polarity, and directional migration, integrating signals from FAK/Src, PI3K–AKT, and MAPK pathways that shape survival and motility programs. Integrin α3β1 also contributes to epithelial organization and barrier integrity by coordinating adhesion-dependent signaling and crosstalk with growth factor receptors. Dysregulated ITGA3 expression and altered integrin signaling have been associated with aberrant invasion and metastatic behavior in multiple cancer contexts, as well as impaired epithelial repair processes in inflammatory and fibrotic settings.

Integrin α3/ITGA3/CD49c CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ITGA3 expression without altering the underlying DNA sequence.

Integrin α3/ITGA3/CD49c CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ITGA3 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 ITGA3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Integrin α3/ITGA3/CD49c expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ITGA3 locus and enabling the study of Integrin α3/ITGA3/CD49c-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Integrin α3/ITGA3/CD49c pathway restoration in tumor cells with silenced or reduced ITGA3 expression.

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