CD40 Lentiviral Activation Particles (m): sc-423444-LAC

Mouse Cd40 encodes CD40, a TNF receptor superfamily member expressed prominently on antigen-presenting cells where it coordinates immune activation through CD40–CD40L interactions. CD40 signaling engages TRAF adaptors to activate NF-κB, MAPK, and PI3K-dependent programs that regulate dendritic cell maturation, B-cell proliferation, germinal center reactions, class-switch recombination, and cytokine production. Through these pathways, CD40 shapes T cell priming and humoral immunity and contributes to inflammatory circuitries relevant to autoimmunity, chronic inflammation, and tumor-associated immune modulation. Perturbation of Cd40 expression is therefore widely studied in models of immune dysregulation, lymphoid biology, and host–pathogen responses.

CD40 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 Cd40 upregulation across a broader range of human cell types.

CD40 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 Cd40 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD40 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Cd40 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.