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
- Glatiramer acetate (GA) is a first-line disease-modifying therapy for multiple sclerosis (MS) with well-established moderate efficacy and high safety, yet its mechanisms of action remain incompletely understood. DNA methylation plays a significant role in MS development and is modulated by various environmental factors, including therapeutic drugs. In this pilot study, we report the first prospective analysis of genome-wide DNA methylation changes in peripheral blood mononuclear cells (PBMCs) from four female relapsing-remitting MS patients before GA initiation and after approximately four and eight months of therapy. We identified 365 loci that are characterized by differential methylation, distinguishing post-treatment time points from baseline, with significant enrichment in CpG islands, shores, and promoter regions. Two distinct temporal patterns emerged: (1) non-monotonic DNA methylation changes peaking at four months and associated with response to foreign antigenic stimuli, and monotonic changes progressively increasing by eight months and related to mTOR-associated pathways relevant to chronic inflammation and neurodegeneration. Integration of DNA methylation and transcriptomic data revealed significant methylation-expression correlations for eight genes, including HLA-, , and -genes with established roles in MS-associated antigen presentation, immunoregulation, and neuroinflammation. Cell composition of PBMCs remained stable throughout treatment. In general, GA therapy for MS appears to induce dynamic, locus-specific DNA methylation changes in PBMCs, with distinct temporal patterns suggesting a biphasic response of the immune system. However, given that none of the individual DMPs reached genome-wide significance, the results presented in this pilot study strongly require validation in larger independent cohorts. Nevertheless, we believe that our findings provide insights into the immunomodulatory effects of GA and lay the foundation for future hypothesis-driven studies to develop epigenetic biomarkers for therapeutic monitoring and generic GA product assessment. - Source: PubMed
Publication date: 2026/05/21
Kiselev IvanKulakova OlgaBaturina OlgaKabilov MarselBoyko AlexeyFavorova Olga - 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