Integrin α2/ITGA2/CD49b CRISPR Activation Plasmid (h): sc-400913-ACT

ITGA2 encodes integrin α2 (CD49b), an adhesion receptor that pairs with integrin β1 to form the α2β1 complex, a major collagen and laminin receptor in many epithelial, endothelial, and immune cell types. By coupling extracellular matrix engagement to intracellular signaling, α2β1 regulates focal adhesion assembly, cytoskeletal remodeling, and mechanotransduction through pathways that include FAK/SRC, PI3K–AKT, and MAPK. ITGA2 activity influences cell migration, platelet adhesion, and tissue remodeling, and altered expression or function has been associated with fibrosis, inflammatory responses, and tumor cell invasion and metastasis. As a surface receptor with context-dependent signaling outputs, ITGA2 is frequently studied in extracellular matrix biology, integrin crosstalk, and cell–matrix interaction models.

Integrin α2/ITGA2/CD49b CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ITGA2 expression without altering the underlying DNA sequence.

Integrin α2/ITGA2/CD49b CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ITGA2 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 ITGA2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Integrin α2/ITGA2/CD49b expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ITGA2 locus and enabling the study of Integrin α2/ITGA2/CD49b-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Integrin α2/ITGA2/CD49b pathway restoration in tumor cells with silenced or reduced ITGA2 expression.

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