Ask about this productRelated genes to: PDE8B antibody
- Gene:
- PDE8B NIH gene
- Name:
- phosphodiesterase 8B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-30
- Date modifiied:
- 2018-07-11
Related products to: PDE8B antibody
Related articles to: PDE8B antibody
- The cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling pathway plays a central role in adrenal function, steroidogenesis, and blood pressure regulation. Increasing evidence suggests that dysregulation of this pathway contributes to several forms of hypertension, both endocrine and non-endocrine. A growing number of germline and somatic alterations affecting components of the cAMP/PKA axis have been implicated as key drivers of hypertensive disorders. Among these, activating pathogenic variants (PV) in , which encodes the stimulatory G protein α-subunit (Gsα) responsible for cAMP production, have been linked to cortisol excess. Mosaic PV , which may present with ACTH-independent Cushing syndrome, while somatic PV have been identified in cortisol-producing adrenal adenomas. Germline inactivating variants in are associated with Furthermore, germline alterations in phosphodiesterases such as and , which impair cAMP degradation, have been associated with Cushing syndrome and micronodular adrenal hyperplasia. Somatic activating PV in , the gene encoding the catalytic subunit of PKA, have also been described in cortisol-producing adenomas. In primary aldosteronism, recent studies-including data from our group-suggest that germline variants in and may contribute to bilateral adrenal hyperplasia and autonomous aldosterone production by modulating intracellular cAMP levels. Additionally, gain-of-function PV in have been associated with a familial form of salt-independent hypertension characterized by enhanced PKA signaling and vascular remodeling. This expanding body of evidence underscores the critical role of the cAMP/PKA pathway in the pathophysiology of distinct hypertensive phenotypes and highlights novel molecular mechanisms and potential therapeutic targets that merit further investigation. - Source: PubMed
Publication date: 2026/02/24
Lima Sobrinho Jose Antonio BAlmeida Madson Q - 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 - Hyperthyroidism and hypothyroidism are globally prevalent endocrine disorders, with their pathogenesis involving multifactorial mechanisms including genetics, immunity, and metabolism. Although genome-wide association studies (GWAS) have identified risk genes such as PDE8B, critical gaps remain in the annotation of causal variants in non-coding regions, characterization of tissue-specific regulatory networks, and understanding of ethnic heterogeneity. This study aimed to systematically identify genes associated with hyperthyroidism and hypothyroidism and unravel their underlying molecular mechanisms through multi-omics integration. - Source: PubMed
Publication date: 2026/01/22
Hu YilangHu HongXu LijunTang XuzhengWang ChongyuLian ZhengyiXie ChenyuXie ZhiwanWang Qingqing - 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 - The nucleic acid metabolism process is driven by various carcinogenic factors, providing a material basis and energy guarantee for the malignant phenotype of tumor cells. However, the role of nucleic acid metabolism in triple-negative breast cancer (TNBC) development remains unclear. Here, we examined the expression patterns of nucleic acid metabolism-related genes (NAMRGs) in the transcriptome of 297 TNBC samples derived from three datasets. We used single-cell RNA sequencing analysis and both in vivo and in vitro experiments to verify the correlation between NAMRGs and tumor metastasis and tumor immune matrix microenvironment (TME) characteristics. According to the results, two different molecular subtypes were identified, and the relationships between the molecular subtypes, four genetic subtypes, and four pathological subtypes were established. Changes in nucleic acid metabolism were related to changes in homologous recombination repair defects (HRD), cell infiltration in the TME, and patient prognosis. We also constructed a prediction model, NAM_model, by including four NAMRGs (DPYD, PDE6G, PDE8B, and TYMS) and integrating it with other clinical indicators. This model was a highly accurate prognostic nomogram, which showed that the prognosis of high-risk patients was poor, with NAMRGs associated with TME immune exhaustion. In addition, NAMRGs were significantly correlated with drug sensitivity to chemotherapy and targeted therapy. In vivo and in vitro studies have shown that PDE8B is an oncogene that promotes tumor growth and induces TNBC metastasis by promoting epithelial-mesenchymal transition (EMT), which has not been reported previously. Single-cell RNA sequencing also revealed the unique effects of nucleic acid metabolism and HRD on exhausted CD8 T cells. A comprehensive analysis of NAMRGs revealed the potential impact of nucleic acid metabolism-mediated mechanisms, such as HRD and EMT, on the clinical pathological characteristics, TME characteristics, and prognosis of patients with TNBC. These findings have deepened our understanding of the roles of NAMRGs in TNBC and immunotherapy, which will greatly contribute to patient stratification management and individualized clinical decision-making. - Source: PubMed
Publication date: 2025/11/06
Yang FanDong YinWu SiqiYou YantingYang YingKong JingweiChen JieChen LiqianJiang XuefengKwan Hiu YeeZhao XiaoshanWang JiLiu Yanyan