Ask about this productRelated genes to: PDE4A antibody
- Gene:
- PDE4A NIH gene
- Name:
- phosphodiesterase 4A
- Previous symbol:
- DPDE2
- Synonyms:
- -
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-29
- Date modifiied:
- 2019-04-16
Related products to: PDE4A antibody
Related articles to: PDE4A antibody
- Hepatocellular carcinoma (HCC), a malignancy of the digestive system, presents limited therapeutic options at advanced stages. In this context, inhibitors of cyclic nucleotide phosphodiesterase 4 (PDE4) have emerged as promising novel agents for patients with advanced HCC. We synthesized a potent PDE4A inhibitor, designated as MG5b, derived from the natural bioactive compound alpha-mangostin, and evaluated its antitumor efficacy in HCC. To assess the impact of MG5b on the proliferation of HCC cells, we conducted MTT and colony formation assays. Flow cytometry was utilized to analyze cell cycle progression, apoptosis, and mitochondrial membrane potential in HCC cells. Intracellular reactive oxygen species (ROS) levels were quantified using a DCF-DA probe. Network pharmacology was employed to predict the associated signaling pathways. Furthermore, Western blotting and immunohistochemistry were utilized to determine the effects of MG5b on protein expression levels. The antitumor efficacy of MG5b was further evaluated in Huh7 xenograft models. MG5b demonstrated a significant inhibitory effect on the proliferation, migration, and invasion of HCC cells, induced cell cycle arrest at the G0/G1 phase, and promoted apoptosis. Mechanistically, MG5b activated the cyclic adenosine monophosphate (cAMP) induced protein kinase A (PKA) signaling pathway, resulting in increased intracellular ROS production and the subsequent suppression of the EGFR-PI3K-AKT pathway. In vivo studies indicated that MG5b markedly inhibited tumor growth while exhibiting minimal toxicity. These findings suggest that MG5b may function as a novel PDE4A inhibitor and hold potential as a promising drug candidate for the treatment of advanced HCC. - Source: PubMed
Publication date: 2026/03/09
Sun ZhitingHuang JieTang YuqinZhang GuoqiangNie ShiqingZhang YanFan ShuranQi MingChen MinfengHe XixinWang JingZhao Jianfu - Phosphodiesterase-4B (PDE4B) regulates intracellular cAMP and drives pro-inflammatory cytokine production. Novel small-molecule PDE4B inhibitors with improved isoform selectivity are needed to broaden therapeutic options. We report the discovery and validation of SIP0401, a ChemBridge-derived small molecule prioritized via an integrated in silico pipeline combining pharmacophore modeling, molecular docking, and dynamics-based scoring. - Source: PubMed
Publication date: 2026/03/10
Alghamdi Uthman MDera Ayed A - Non-POU domain containing octamer binding protein (NONO) is a multifunctional nuclear protein which plays important roles in regulating nuclear processes such as transcription and splicing. However, the role of NONO played in regulating airway smooth muscle (ASM) contraction remains largely unknown. In this study, we aimed to delineate the effects and the underlying mechanisms of NONO on ASM contraction. By deploying NONO gene knockout (NONO K.O.) mice, we examined tracheal contractility using a mechanical recording system. The expression of PDE4 was quantified by real-time PCR, the contents of IP, calmodulin, cAMP, myosin light chain kinase (MLCK) and phosphorylated MLC (p-MLC) were determined through ELISA. The results showed a significant decline of ASM contractility in NONO K.O. mice compared with wild type (W.T.), PDE inhibitor IBMX and PDE4 inhibitor rolipram largely attenuated the decreased ASM contraction of NONO K.O. mice. PDE4A-C mRNA expression were up-regulated while basal level of cAMP, calmodulin and IP declined in NONO K.O. mice. Furthermore, two important components of the contractile apparatus, MLCK and p-MLC, were also decreased after carbachol (CCh) stimulation. These data demonstrated that NONO was capable of regulating ASM contraction through, at least partially, PDE4/cAMP signaling pathways and provided a novel regulatory target of ASM contractility. - Source: PubMed
Publication date: 2026/02/14
Fang Xiao-MinNiu YaHu DanZhang Xiu-JuanZhang Rui-Gang - Cordyceps sinensis (CS) is a fungus that parasitizes the larvae and corpses of Batmadaceae insects. CS is used as a traditional Chinese medicine and has shown promising clinical efficacy in the treatment of chronic obstructive pulmonary disease (COPD). This study aimed to identify potential targets of CS in the treatment of COPD and to analyse the related biological processes and signalling pathways. - Source: PubMed
Zang ZiruiKong YuhanKong Qi - Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are chronic autoimmune diseases characterized by persistent inflammation and progressive tissue damage, posing significant challenges to effective treatment. To gain deeper insights into their shared molecular mechanisms, we performed an integrative bioinformatics investigation aimed at uncovering common pathways and therapeutic targets. Using a cutoff of p-value < 0.05 and Log2 FC > 1, differential gene expression analysis identified 1178 DEGs in RA and 7783 DEGs in SLE, with 358 genes common to both diseases. Construction of a protein-protein interaction network revealed several hub genes, including , and , which were highly interconnected and clustered into functional modules. Molecular docking analysis demonstrated that alpha linolenic acid (ALA) exhibited strong binding affinity toward these key proteins, with binding energies ranging from -8.3 to -9.4 kcal/mol. Toxicity profiling further suggested that ALA possesses a favorable safety profile, showing minimal risks of hepatotoxicity, neurotoxicity, and related adverse outcomes. Functional enrichment pointed to the involvement of common signaling cascades, particularly the cAMP and TGF-β pathways, as potential therapeutic avenues. Collectively, our findings highlight ALA as a promising therapeutic candidate capable of modulating shared molecular drivers in RA and SLE. Further in vitro and in vivo validation is essential to confirm its mechanistic effects and therapeutic potential for clinical translation. - Source: PubMed
Publication date: 2025/11/01
Naveed MuhammadAli Syed MurtazaAziz TariqMakhdoom Syeda IzmaCheema Sana RehmanAlkhateeb Mariam AbdulazizAlwethaynani Maher SAlsulami Seham OSagini Hanan AbdulrahmanMansouri Omniah A