Ask about this productRelated genes to: PDE5A antibody
- Gene:
- PDE5A NIH gene
- Name:
- phosphodiesterase 5A
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4q26
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-24
- Date modifiied:
- 2016-10-05
Related products to: PDE5A antibody
Related articles to: PDE5A antibody
- The extensive application of bisphenol A (BPA), an endocrine-disrupting substance in polymer-based products and consumer commodities, has sparked concerns over its carcinogenic potential. However, the molecular mechanisms underlying BPA-induced gastric carcinogenesis remain poorly understood. We used network toxicology and molecular docking analysis to uncover the pivotal targets and mechanisms underlying BPA-associated gastric carcinogenesis. Potential BPA-related targets and differentially expressed genes in gastric cancer (GC) were collected from publicly available databases to identify hub genes. A prognostic risk assessment model utilizing hub genes, with molecular docking simulations, was performed to confirm the binding interactions between BPA and target proteins. A total of 27 potential targets associated with both BPA exposure and GC were identified. The protein-protein interaction network analysis revealed 19 hub genes, with core targets including MMP9, ADRB2, PTGS1, SLC6A4, ERBB2, MAPT, AR, SLC6A3, CNR1, PDE5A, DRD2, KCNH2, MC4R, CALCR, CHRM1, ADRB3, CXCR2, MMP1, and SHBG. Enrichment analysis demonstrated these hub genes were significantly involved in neuroactive ligand-receptor interaction, calcium signaling pathway, cGMP-PKG signaling pathway, and chemical carcinogenesis-receptor activation pathways. Prognostic analysis identified six hub genes (CALCR, ADRB3, CNR1, HRH2, KCNH2, and AR) significantly associated with patient survival. Molecular docking simulations demonstrated robust interaction affinities of BPA with the identified core target proteins. This study reveals that BPA may influence GC development and progression through multiple targets and signaling pathways, particularly involving G protein-coupled receptor signaling, hormone regulation, and neurological pathways. - Source: PubMed
Publication date: 2026/05/14
Yu Wen-YanZhang Yue - Sarcopenic obesity (SO) is a complex condition involving increased fat accumulation along with reduced muscle mass and impaired muscle function; however, there are currently no approved pharmacological interventions targeting these pathological features. Akt and AMPK are key signaling pathways regulating muscle homeostasis and energy metabolism. Natural compounds that modulate these pathways may offer a promising multi-targeted therapeutic strategy. This study investigated the effects of Fucoidan P on SO and its underlying molecular pathways, while assessing translational relevance using clinical datasets. Fucoidan P decreased body weight and fat mass and size while improving grip strength, muscle mass, and fiber size during high-fat diet feeding. Fucoidan P mitigated muscle atrophy through phosphorylation of Akt, mTOR, and FOXO3a, and enhanced energy metabolism by activating the AMPK/SIRT1/PGC-1α pathway. Moreover, Fucoidan P downregulated PDE5A and PTGS1, which are identified differentially expressed genes-related to inflammation of clinical datasets, and inhibited pro-inflammatory cytokines by suppressing NF-κB pathway. Taken together, these findings demonstrate that Fucoidan P alleviates SO by coordinately regulating muscle protein homeostasis, energy metabolism, and inflammatory responses through a network of interconnected Akt and AMPK/PGC-1α, and NF-κB signaling pathways, suggesting its potential as a multi-target therapeutic agent for SO. - Source: PubMed
Publication date: 2026/04/08
Kim Jong-YeonKim Sung-MinLee SanghoonJeon Ju-HongPark Eun-JungLee Hae-Jeung - Cadmium (Cd) is a well-recognized neurotoxic metal whose effects on the central nervous system accumulate with both exposure intensity and duration. However, how dose and time jointly sculpt brain proteome trajectories-and which early molecular events emerge under low-dose, short-duration exposure-remain insufficiently resolved. Time-resolved proteomics can map these trajectories, but requires explicit dose-time deconvolution to separate main effects from interaction-driven changes while accounting for biological heterogeneity. - Source: PubMed
Publication date: 2026/05/02
Hu ZhijianHan FengGao HaoWan ShengLiu HuiJie LiYin YinghuiTian MaoqinYang YongChen WenjieTan XiaoShi XinxinChen QiwenHuang Shaoxin - to investigate the therapeutic effects of vildagliptin on non-valvular atrial fibrillation (NVAF) and to determine whether its underlying mechanism of action is associated with modulation of the nitric oxide/soluble guanylate cyclase/cyclic guanosine monophosphate (NO/sGC/cGMP) signaling pathway. - Source: PubMed
Publication date: 2026/04/29
Wang ZhaodiZhao ZhihanZang XiaobiaoWang LeiZhao Yonghui - - Source: PubMed
Publication date: 2026/04/22
Prakash Siddharth K