Integrin αE/ITGAE/CD103 CRISPR Activation Plasmid (h): sc-404333-ACT

ITGAE encodes integrin αE (CD103), which pairs with integrin β7 to form the αEβ7 heterodimer that binds E-cadherin and promotes adhesion and retention of lymphocytes within epithelial tissues. This receptor is prominent on tissue-resident memory T cells, subsets of regulatory T cells, and mucosal dendritic cells, supporting immune surveillance, cell localization, and immune synapse formation. CD103-dependent interactions influence leukocyte trafficking, epithelial barrier immunity, and inflammatory signaling in mucosal microenvironments. Altered ITGAE/CD103 expression is frequently used to stratify immune cell states in contexts such as intestinal inflammation, transplant-associated immune responses, and tumor-infiltrating lymphocyte phenotypes.

Integrin αE/ITGAE/CD103 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ITGAE expression without altering the underlying DNA sequence.

Integrin αE/ITGAE/CD103 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ITGAE 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 ITGAE transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Integrin αE/ITGAE/CD103 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ITGAE locus and enabling the study of Integrin αE/ITGAE/CD103-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Integrin αE/ITGAE/CD103 pathway restoration in tumor cells with silenced or reduced ITGAE expression.

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