CD1C CRISPR Activation Plasmid (h): sc-403813-ACT

CD1C (CD1c molecule) is a non-classical MHC class I–like antigen-presenting glycoprotein predominantly expressed on dendritic cell subsets and certain B cells, where it binds and displays lipid and glycolipid antigens to T cells. By mediating presentation of microbial and self-lipid ligands, CD1C contributes to initiation and shaping of adaptive immune responses and influences cytokine polarization in the context of antigen processing and presentation pathways. CD1C-positive dendritic cells participate in pathogen sensing and crosstalk with innate immune programs, linking lipid antigen availability to T cell activation and immune homeostasis. Altered CD1C expression or CD1c-restricted immune recognition has been investigated in inflammatory and autoimmune conditions, infectious disease responses, and tumor-associated immune remodeling.

CD1C CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CD1C expression without altering the underlying DNA sequence.

CD1C CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CD1C 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 CD1C transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD1C expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CD1C locus and enabling the study of CD1C-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD1C pathway restoration in tumor cells with silenced or reduced CD1C expression.

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