CD52 CRISPR Activation Plasmid (h): sc-403151-ACT

CD52 encodes a small glycosylphosphatidylinositol (GPI)-anchored glycoprotein displayed at high density on the surface of many hematopoietic cells, including lymphocytes and monocytes. Through its membrane anchoring and localization to lipid microdomains, CD52 participates in cell–cell interactions and can influence immune cell activation states and signaling processes linked to leukocyte function. CD52 expression is widely used to define immune cell subsets and to study mechanisms governing immune homeostasis and inflammatory responses. Altered CD52 expression patterns have been reported across immune-mediated disorders and hematologic malignancies, supporting its relevance for investigating immune regulation in disease contexts.

CD52 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CD52 expression without altering the underlying DNA sequence.

CD52 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CD52 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 CD52 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CD52 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CD52 locus and enabling the study of CD52-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CD52 pathway restoration in tumor cells with silenced or reduced CD52 expression.

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