Integrin αX/ITGAX/CD11c Lentiviral Activation Particles (m): sc-421170-LAC

Itgax encodes integrin αX (CD11c), which heterodimerizes with integrin β2 (CD18) to form complement receptor 4 (CR4), a key adhesion and phagocytic receptor on myeloid lineages including dendritic cells, macrophages, and subsets of monocytes. CD11c participates in leukocyte adhesion, migration, and immune synapse formation through interactions with ligands such as iC3b and ICAMs, linking extracellular cues to cytoskeletal remodeling and downstream signaling pathways that shape antigen uptake and presentation. In mouse immunology, ITGAX is widely used as a marker and functional regulator of dendritic cell differentiation and tissue trafficking, with relevance to inflammatory responses and immune dysregulation in models of autoimmunity, infection, and tumor immunology. Perturbing Itgax expression helps interrogate myeloid cell activation states, antigen-presenting cell function, and complement-dependent clearance mechanisms in vivo and in vitro.

Integrin αX/ITGAX/CD11c Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Itgax upregulation across a broader range of human cell types.

Integrin αX/ITGAX/CD11c Lentiviral Activation Particles (m) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the Itgax transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Integrin αX/ITGAX/CD11c expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Itgax genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

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