
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PKAγ cat CRISPR Activation Plasmid (h) | sc-400874-ACT | 20 µg | $397.00 |
PRKACG encodes the catalytic gamma subunit of cAMP-dependent protein kinase A (PKA), a core effector of GPCR–adenylyl cyclase signaling that phosphorylates diverse substrates to regulate metabolism, cytoskeletal dynamics, ion channel activity, and transcriptional programs such as CREB-dependent gene expression. Through cAMP/PKA signaling, PRKACG participates in signal integration across pathways including MAPK, calcium-dependent responses, and regulation of cell cycle and differentiation. Dysregulated PKA activity and altered cAMP signaling are implicated in oncogenic signaling, endocrine and metabolic dysfunction, and disorders of neuronal and cardiac excitability, making PRKACG a useful node for mechanistic studies of pathway rewiring.
PKAγ cat CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PRKACG expression without altering the underlying DNA sequence.
PKAγ cat CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PRKACG 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 PRKACG transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PKAγ cat expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PRKACG locus and enabling the study of PKAγ cat-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PKAγ cat pathway restoration in tumor cells with silenced or reduced PRKACG expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.