CD55 Lentiviral Activation Particles (h): sc-400738-LAC

CD55 (decay-accelerating factor, DAF) is a glycosylphosphatidylinositol-anchored cell-surface regulator of the complement cascade that disrupts C3/C5 convertases to limit complement amplification on host membranes. By controlling complement activation, CD55 influences innate immune surveillance, inflammatory signaling, and cell–cell interactions at the immunological synapse, and it can modulate susceptibility to complement-dependent stress. Altered CD55 expression has been associated with immune dysregulation and inflammatory pathobiology, and it is frequently studied in the context of complement-mediated tissue injury and tumor immune evasion mechanisms. As a broadly expressed membrane protein, CD55 is also used as a marker in studies of cell-surface glycoprotein trafficking and microdomain organization.

CD55 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 CD55 upregulation across a broader range of human cell types.

CD55 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 CD55 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD55 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CD55 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.