
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CD163 CRISPR Activation Plasmid (h) | sc-400435-ACT | 20 µg | $397.00 |
CD163 encodes a macrophage-restricted scavenger receptor of the SRCR family that binds hemoglobin–haptoglobin complexes and mediates their endocytosis, linking heme detoxification to anti-oxidant and iron-handling programs. CD163 is enriched on monocytes and tissue macrophages and is associated with anti-inflammatory polarization, modulating cytokine signaling networks such as IL-10–responsive pathways and responses to innate immune stimuli. By shaping clearance of extracellular hemoglobin and remodeling inflammatory tone, CD163 influences macrophage activation states within infection, atherosclerosis, and tumor-associated microenvironments. Altered CD163 expression is frequently used as a marker of macrophage infiltration and phenotype in studies of chronic inflammation and immune dysregulation.
CD163 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CD163 expression without altering the underlying DNA sequence.
CD163 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CD163 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 CD163 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD163 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CD163 locus and enabling the study of CD163-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD163 pathway restoration in tumor cells with silenced or reduced CD163 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.