Ask about this productRelated genes to: PDE7A antibody
- Gene:
- PDE7A NIH gene
- Name:
- phosphodiesterase 7A
- Previous symbol:
- -
- Synonyms:
- HCP1
- Chromosome:
- 8q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-21
- Date modifiied:
- 2016-11-01
Related products to: PDE7A antibody
Related articles to: PDE7A antibody
- Epithelial-mesenchymal transition (EMT) is a key driver of idiopathic pulmonary fibrosis (IPF), yet therapies specifically targeting epithelial cells remain limited. The role of phosphodiesterase 7A (PDE7A) in IPF and its mechanism in regulating EMT are still largely unknown. This study aims to investigate the anti-fibrotic effect of BRL-50481, focusing on its target PDE7A and the associated molecular mechanism in regulating epithelial cell fibrosis and EMT. BRL-50481 was identified as a top candidate compound targeting pathogenic alveolar epithelial cells through bioinformatic screening. Its efficacy was evaluated in both a bleomycin-induced murine pulmonary fibrosis model and a TGF-β-induced A549 cell model. Drug-target interaction was characterized using molecular docking, cellular thermal shift assay (CETSA), and site-directed mutagenesis. Downstream signaling pathways were predicted via the TRRUST database and experimentally validated. PDE7A was found to be highly expressed in alveolar epithelial cells of IPF patients and mice. BRL-50481 directly bound to the ILE323 residue of PDE7A, specifically inhibiting JAK2/STAT3 signaling pathway activation. This inhibition suppressed EMT, inflammatory factor release, and collagen deposition, ultimately alleviating pulmonary fibrosis in both in vivo and in vitro models. PDE7A acts as a key upstream regulator driving JAK2/STAT3 signaling activation and the EMT process in alveolar epithelial cells. BRL-50481 exerts anti-fibrotic effects by precisely targeting this mechanism, providing novel insights into IPF pathogenesis and establishing a theoretical foundation for developing innovative therapies targeting PDE7A. - Source: PubMed
Publication date: 2026/02/10
Guo JianqiangZhou JiaweiCheng AnqiHu WeinanQi TianxiangZhao DahaiBai YingHu DongWu Jing - Spermatogenesis is a complex process of cell differentiation preceded and accompanied by distinct gene expressions that lead to a variety of cellular and physiological changes. By degrading cyclic adenosine 3',5'-monophosphate (cAMP), some phosphodiesterases contribute to spermatogenesis by modulating signal transduction across various physiological processes. Although phosphodiesterase 7A (PDE7A) degrades cAMP; its function in the testis as a regulator remains unclear. Furthermore, the exact cell types that express PDE7A at different stages of testicular development remain unknown. - Source: PubMed
Publication date: 2025/11/30
Osta Narjes M ElEl-Mabrouk Zainab H - 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 - Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer, associated with poor response to therapies and high mortality. We identify that phosphodiesterase 7A (PDE7A) is overexpressed in the majority of TNBCs, and a higher level of PDE7A associates with poor prognosis. The phosphatidylinositol 3-kinase (PI3K)/AKT pathway, via the transcription factor IRF1, stimulates the expression of PDE7A in TNBC cells. PDE7A inhibition attenuates TNBC growth in both cell culture and mouse models of TNBC. Inhibition of PDE7A suppresses de novo pyrimidine biosynthesis, in part through the downregulation of the enzyme dihydroorotate dehydrogenase (DHODH). DHODH suppression attenuates TNBC tumor growth, mirroring the effects of PDE7A inhibition, and ectopic DHODH expression rescues PDE7A-inhibition-induced tumor suppression. Pharmacological co-targeting of PDE7A and DHODH potently inhibits TNBC tumor growth and metastasis. These findings identify the PDE7A → DHODH →de novo pyrimidine biosynthesis pathway as a key driver of TNBC, offering additional therapeutic opportunities for TNBC patients. - Source: PubMed
Malvi ParmanandBugide SureshDutta RoshanReddi Kiran KumarEdwards Yvonne J KSingh KamaljeetGupta RomiWajapeyee Narendra