Integrin αX/ITGAX/CD11c CRISPR Activation Plasmid (h): sc-401765-ACT

ITGAX encodes integrin αX (CD11c), an α subunit that heterodimerizes with integrin β2 (CD18) to form complement receptor 4 (CR4), a key adhesion and phagocytic receptor on myeloid lineage cells. CD11c mediates cell–cell and cell–matrix interactions, leukocyte trafficking, and complement-dependent recognition of iC3b-opsonized targets, integrating cues from inside-out integrin signaling to regulate cytoskeletal remodeling and immune synapse formation. Through coordinated crosstalk with Fc receptor signaling and downstream kinase networks, ITGAX influences antigen uptake, dendritic cell maturation, and inflammatory cytokine programs. Dysregulated ITGAX expression or CD11c+ cell abundance is frequently used to stratify immune infiltration and myeloid activation states in cancer, autoimmune inflammation, and chronic infectious settings, supporting mechanistic studies of myeloid-driven disease biology.

Integrin αX/ITGAX/CD11c CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ITGAX expression without altering the underlying DNA sequence.

Integrin αX/ITGAX/CD11c CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ITGAX 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 ITGAX transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Integrin αX/ITGAX/CD11c expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ITGAX locus and enabling the study of Integrin αX/ITGAX/CD11c-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Integrin αX/ITGAX/CD11c pathway restoration in tumor cells with silenced or reduced ITGAX expression.

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