
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DEC-205 CRISPR Activation Plasmid (h) | sc-417220-ACT | 20 µg | $397.00 |
LY75 encodes DEC-205 (CD205), a C-type lectin endocytic receptor highly expressed by dendritic cell subsets and thymic epithelial cells, where it supports efficient uptake and routing of extracellular ligands to antigen-processing compartments. Through receptor-mediated endocytosis and delivery to MHC class II and cross-presentation pathways, DEC-205 helps shape T cell priming, peripheral tolerance, and thymic selection. Its expression and trafficking intersect with vesicular transport, lysosome-dependent processing, and immune synapse biology. Dysregulated antigen handling and altered DEC-205 distribution have been studied in the context of inflammation, autoimmunity, and tumor-associated immune modulation as biomarkers of antigen-presenting cell state.
DEC-205 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LY75 expression without altering the underlying DNA sequence.
DEC-205 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LY75 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 LY75 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DEC-205 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LY75 locus and enabling the study of DEC-205-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DEC-205 pathway restoration in tumor cells with silenced or reduced LY75 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.