CD38 Lentiviral Activation Particles (h): sc-401117-LAC

Human CD38 encodes a type II transmembrane ectoenzyme and receptor that catalyzes NAD+ metabolism to generate second messengers such as cyclic ADP-ribose and ADP-ribose, thereby regulating intracellular Ca2+ mobilization. CD38 activity integrates metabolic state with signaling processes that influence lymphocyte activation, differentiation, adhesion, and cytokine responses, with additional roles in cellular redox balance through NAD+-dependent pathways. CD38 is prominently expressed in immune cell subsets and is frequently studied in the context of immunometabolism, inflammatory signaling, and tumor–immune interactions. Dysregulated CD38 expression or enzymatic function has been associated with altered immune homeostasis and microenvironmental signaling in hematologic malignancies and other diseases where NAD+ consumption and Ca2+-dependent signaling are perturbed.

CD38 Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient CD38 upregulation across a broader range of human cell types.

CD38 Lentiviral Activation Particles (h) 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 CD38 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD38 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CD38 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.