CD69 Lentiviral Activation Particles (h2): sc-416315-LAC-2

Human CD69 encodes CD69, a type II transmembrane C-type lectin receptor rapidly induced on activated T cells, B cells, NK cells, and other leukocytes, where it functions as an early activation marker and modulator of immune signaling. CD69 influences lymphocyte trafficking and tissue retention through regulation of sphingosine-1-phosphate receptor 1 (S1PR1) and contributes to downstream programs affecting cytokine production, proliferation, and immune synapse dynamics. Through its roles in immune activation, mucosal and tissue-resident immunity, and inflammatory signaling networks, CD69 is implicated in immune dysregulation observed in autoimmunity, chronic inflammation, infection, and tumor immune microenvironments. Gene editing or functional perturbation of CD69 in human cells supports mechanistic studies of activation-dependent transcriptional circuits, migration/egress control, and immune cell phenotyping in in vitro and ex vivo research models.

CD69 Lentiviral Activation Particles (h2) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient CD69 upregulation across a broader range of human cell types.

CD69 Lentiviral Activation Particles (h2) 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 CD69 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD69 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CD69 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.