CD33 Lentiviral Activation Particles (h): sc-401011-LAC

Human CD33 encodes a sialic acid–binding immunoglobulin-like lectin (Siglec-3) predominantly expressed on cells of the myeloid lineage, where it functions as an inhibitory receptor that shapes innate immune activation. Upon ligand engagement, CD33 signals through ITIM-dependent recruitment of phosphatases such as SHP-1/2, modulating downstream pathways including PI3K/AKT and MAPK to regulate cytokine output, phagocytosis, and antigen presentation. CD33 is widely used as a marker of myeloid differentiation and has strong relevance to hematologic malignancies and neuroinflammatory biology, including microglial programs linked to Alzheimer’s disease risk. Altered CD33 expression or signaling can shift immune checkpoint tone in myeloid cells, influencing inflammatory set points and tissue remodeling.

CD33 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 CD33 upregulation across a broader range of human cell types.

CD33 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 CD33 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD33 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CD33 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.