
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PTG CRISPR Activation Plasmid (h) | sc-404419-ACT | 20 µg | $397.00 |
PPP1R3C encodes protein targeting to glycogen (PTG), a regulatory subunit that recruits protein phosphatase 1 to glycogen particles and coordinates dephosphorylation of key enzymes controlling glycogen synthesis and breakdown. By scaffolding phosphatase activity near glycogen-metabolic complexes, PTG helps tune cellular glucose storage, energy homeostasis, and signaling cross-talk with nutrient-sensitive pathways. Altered PPP1R3C expression or PTG function has been linked to dysregulated glycogen accumulation and metabolic phenotypes relevant to insulin-responsive tissues. As a result, PPP1R3C is widely studied in models of glucose handling, stress adaptation, and tissue-specific metabolic regulation.
PTG CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PPP1R3C expression without altering the underlying DNA sequence.
PTG CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PPP1R3C 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 PPP1R3C transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PTG expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PPP1R3C locus and enabling the study of PTG-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PTG pathway restoration in tumor cells with silenced or reduced PPP1R3C expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.