CD163 CRISPR Activation Plasmid (m): sc-429989-ACT

Mouse Cd163 encodes CD163, a macrophage-restricted scavenger receptor of the SRCR family that binds hemoglobin–haptoglobin complexes and promotes their endocytosis, supporting heme catabolism and iron recycling through the HO-1 pathway. CD163 is a hallmark of alternatively activated (M2-like) macrophages and participates in clearance programs that shape inflammatory resolution, cytokine networks, and tissue remodeling. Its expression is modulated by inflammatory cues and intersects with innate immune signaling and phagocytic trafficking, influencing macrophage polarization states. Altered CD163 levels are frequently used to contextualize macrophage involvement in chronic inflammation, fibrotic remodeling, metabolic dysfunction, infection, and tumor-associated macrophage biology in mouse models.

CD163 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Cd163 expression without altering the underlying DNA sequence.

CD163 CRISPR Activation Plasmid (m) 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.