Ask about this productRelated genes to: PDE8A Blocking Peptide
- Gene:
- PDE8A NIH gene
- Name:
- phosphodiesterase 8A
- Previous symbol:
- -
- Synonyms:
- HsT19550
- Chromosome:
- 15q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-12
- Date modifiied:
- 2014-11-19
Related products to: PDE8A Blocking Peptide
Related articles to: PDE8A Blocking Peptide
- Phosphodiesterases (PDEs) constitute a superfamily of enzymes comprising 11 distinct families that hydrolyze cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), thereby precisely regulating the spatiotemporal dynamics of intracellular cyclic nucleotides. Among these PDEs, PDE8 is distinguished by its high affinity and specificity for cAMP and exerts diverse biological effects. The PDE8 family comprises two genes, Pde8a and Pde8b, which are widely distributed throughout the brain and are expressed in both neuronal and glial cells. The widespread distribution of PDE8 in the brain suggests its involvement in roles of the central nervous system (CNS). In this context, dysregulation of PDE8 has been implicated in the pathogenesis of several CNS diseases, including neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. This review aimed to enhance the understanding of the role of PDE8 in the mechanisms underlying neurodegenerative diseases, while providing a theoretical foundation and potential avenues for developing novel therapeutic strategies. - Source: PubMed
Publication date: 2026/06/06
Zhao XuanFu Yi-TingQiu Nian-ZhuangPan Yu-XuanZhang Han-TingWang Hao - Osteocytes are the primary mechano-sensitive cell type in bone. Mechanical loading is sensed across the dendritic projections of osteocytes leading to transient reductions in focal adhesion kinase (FAK) activity. We performed tyrosine-focused phospho-proteomic profiling in osteocyte-like Ocy454 cells to identify FAK substrates. Gsα, parathyroid hormone receptor (PTH1R), and phosphodiesterase 8A (PDE8A), three proteins associated with cAMP signaling, were found as potential FAK targets. FAK pharmacologic inhibition or gene deletion increased basal and G-protein-coupled-receptor (GPCR) ligand-stimulated cAMP levels and downstream signaling events. PDE8A inhibition mimicked FAK inhibition at the levels of increased cAMP, protein kinase A (PKA) activity, and expression of cAMP-regulated target genes. Co-immunoprecipitation assays revealed an intracellular association between FAK and PDE8A. Thus, mechanically regulated FAK can modulate intracellular cAMP levels via effects on PDE8A. These data suggest a signal transduction mechanism that mediates crosstalk between mechanical and cAMP-linked hormonal signaling in osteocytes. - Source: PubMed
Publication date: 2026/05/22
Papaioannou GaryfalliaSato TadatoshiHoughton CarolineYan ChuanqingKotsalidis Parthena EStrauss Katelyn EDean ThomasMazur Courtney MNelson Alissa JStokes Matthew PGardella Thomas JWein Marc N - Phosphodiesterases (PDEs) are considered promising drug targets due to their close association with various pathological and physiological processes. We aimed to investigate the causal relationship between PDE inhibitors and hypertensive disorders of pregnancy (HDP) and fetal growth restriction (FGR). - Source: PubMed
Publication date: 2026/05/20
Xia DandanLi SiyuLiu WenjieZhang YuhuiZhang ChenyingShe GuangtongWang Huiyan - Thoracic aortic aneurysm (TAA) is driven by complex molecular mechanisms beyond size thresholds, yet the role of cyclic nucleotide metabolism remains unclear. Phosphodiesterases (PDEs), which hydrolyze cAMP and cGMP in compartmentalized microdomains, act as key regulators of vascular integrity and remodeling. - Source: PubMed
Publication date: 2026/01/01
Magouliotis Dimitrios ESicouri SergeAndroutsopoulou VasilikiBaudo MassimoCabrucci FrancescoZotos Prokopis-AndreasXanthopoulos AndrewRamlawi Basel - Dysregulation in the production of cyclic nucleotides and the upregulation of cyclic nucleotide phosphodiesterases (PDEs) are implicated in many tumor pathologies. Therefore, a comprehensive investigation of PDEs and their dysfunction across different cancers is necessary. In this study, we conducted an in-depth analysis of the genomic expression and variation profiles of PDEs across multiple cancer types. We found that PDE6C, PDE6D, PDE6H, and PDE7A were significantly upregulated in nearly all types of cancer, whereas PDE2A was downregulated in 15 cancer types. Our results demonstrated that somatic copy number alterations (SCNAs) and promoter DNA methylation in pan-cancer samples were heterogeneous and may regulate the expression of PDEs in tumors. We further observed that the expression of PDEs predominantly influences the prognosis of solid tumors. Five differentially expressed PDEs (PDE5A, PDE6D, PDE8A, PDE8B, and PDE9A) were identified as independent prognostic factors for patients with pan-cancer in both the training and testing cohorts. To our knowledge, this is the first study to construct a PDE signature in pan-cancer and to highlight the pivotal role of PDE4D in LIHC (liver hepatocellular carcinoma). - Source: PubMed
Publication date: 2025/12/12
Wu ZenghongRen HuiliGuo Feng