CD206/Mannose Receptor/MMR CRISPR Activation Plasmid (h): sc-400286-ACT

MRC1 encodes CD206, also known as the macrophage mannose receptor (MMR), a type I transmembrane C-type lectin predominantly expressed by macrophages and dendritic cell subsets. CD206 binds mannose-, fucose-, and N-acetylglucosamine–containing glycans on endogenous and microbial ligands, supporting receptor-mediated endocytosis, phagocytosis, and antigen processing. Through roles in scavenging, glycan recognition, and clearance of glycoproteins, MRC1 contributes to innate immune sensing and modulation of inflammatory polarization programs. Altered CD206 expression is frequently used as a marker of alternatively activated macrophages and has been associated with immune microenvironment remodeling in chronic inflammation, fibrosis, and tumor biology.

CD206/Mannose Receptor/MMR CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MRC1 expression without altering the underlying DNA sequence.

CD206/Mannose Receptor/MMR CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MRC1 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.

Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the MRC1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD206/Mannose Receptor/MMR expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MRC1 locus and enabling the study of CD206/Mannose Receptor/MMR-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD206/Mannose Receptor/MMR pathway restoration in tumor cells with silenced or reduced MRC1 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.