PAcP CRISPR Activation Plasmid (h): sc-405118-ACT

Human ACPP encodes prostatic acid phosphatase (PAcP), a secreted and intracellular phosphomonoesterase that modulates phosphate-dependent signaling and cellular differentiation programs. In prostate epithelium, PAcP has been linked to regulation of tyrosine phosphorylation states and downstream pathways that influence androgen-responsive transcription and growth control. Altered ACPP/PAcP expression and activity are frequently studied in the context of prostate biology, including changes associated with tumor progression and cellular plasticity. As a tissue-enriched marker with functional signaling roles, ACPP provides a useful entry point for dissecting phosphatase-driven network remodeling in cancer-relevant models.

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

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

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