
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PDE10A CRISPR Activation Plasmid (h) | sc-403981-ACT | 20 µg | $397.00 |
Human PDE10A encodes phosphodiesterase 10A, a dual-substrate phosphodiesterase that hydrolyzes cAMP and cGMP to tune cyclic nucleotide signaling dynamics. By shaping second-messenger tone, PDE10A regulates PKA and PKG pathway output, influencing phosphorylation-dependent transcriptional programs, ion channel activity, and synaptic signaling. PDE10A is highly implicated in neuronal signaling networks, where altered cyclic nucleotide homeostasis is associated with neuropsychiatric and neurodegenerative disease biology. Its pathway position also makes it a useful node for studying cross-talk between GPCR signaling, intracellular kinase cascades, and context-dependent gene expression.
PDE10A CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PDE10A expression without altering the underlying DNA sequence.
PDE10A CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PDE10A 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 PDE10A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PDE10A expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PDE10A locus and enabling the study of PDE10A-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PDE10A pathway restoration in tumor cells with silenced or reduced PDE10A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.