CD206/Mannose Receptor/MMR Lentiviral Activation Particles (m): sc-421707-LAC

Mrc1 encodes CD206/Mannose Receptor (MMR), a macrophage- and dendritic cell–enriched C-type lectin scavenger receptor that binds mannose-, fucose-, and N-acetylglucosamine–containing glycans on pathogens and endogenous glycoproteins. CD206 mediates clathrin-dependent endocytosis and phagocytosis, supporting antigen uptake and processing, lysosomal trafficking, and glycan-driven recognition in innate immunity. It is widely used as a marker of alternatively activated (M2-like) macrophage polarization and participates in pathways shaping tissue remodeling, wound repair, and immunoregulatory cytokine programs. Altered CD206 expression is implicated in chronic inflammation, fibrosis, metabolic dysfunction, and tumor-associated macrophage biology, making Mrc1 relevant for studies of microenvironmental regulation and host–pathogen interactions in mouse models.

CD206/Mannose Receptor/MMR 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 Mrc1 upregulation across a broader range of human cell types.

CD206/Mannose Receptor/MMR 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 Mrc1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD206/Mannose Receptor/MMR expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Mrc1 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.