Ask about this productRelated genes to: PDE1A Blocking Peptide
- Gene:
- PDE1A NIH gene
- Name:
- phosphodiesterase 1A
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-05
- Date modifiied:
- 2015-11-18
Related products to: PDE1A Blocking Peptide
Related articles to: PDE1A Blocking Peptide
- Metabolic perturbations in the tumor microenvironment profoundly compromise the stemlike properties and effector functions of CD8 T cells. Deciphering the metabolic circuitry that sustains T cell stemness is critical for reinvigorating tumor-infiltrating lymphocytes and augmenting immunotherapeutic efficacy. Here, we identify citraconate, an itaconate isomer, as a metabolite markedly depleted in CD8 T cells subjected to chronic antigen stimulation or hypoxic conditions. Citraconate supplementation preserves stemlike characteristics, attenuates ferroptosis, and potentiates T cell-mediated antitumor immunity. Mechanistically, citraconate maintains intracellular cyclic adenosine monophosphate (cAMP) concentrations by suppressing phosphodiesterase1A/C (PDE1A/C) expression and preserving mitochondrial integrity, thereby activating protein kinase A (PKA) signaling. This activation transcriptionally represses arachidonate-5-lipoxygenase (ALOX5), consequently reducing arachidonic acid peroxidation. Clinically, diminished ALOX5 or PDE1A expression correlates with reduced T cell exhaustion and improved responses to immune checkpoint blockade (ICB) therapy. Our findings reveal the citraconate-mediated PDE1-cAMP-ALOX5 axis as a potential therapeutic target for enhancing cancer immunotherapy. - Source: PubMed
Publication date: 2026/05/01
Li WenhuiGe MinminLuo ZiyiNi MinjuTang KexinHan ChenfengWang JiajiaMa YifuLiu XiaoweiMa KailiYang JingxingLi WenjingZhang CangangZhao QitaiShao GuangcanPark JaeohZhang YiWan YonghongZhang BaojunWang GangShen MingjingShan QiangGuo FengHo Ping-ChihZhang LiyuanZhang Lianjun - Pirfenidone, an antifibrotic agent, has been shown to be effective in the treatment of idiopathic pulmonary fibrosis (IPF). However, the exact mechanism of action and clinical efficacy require further investigation and validation. This study commenced by identifying pathogenic genes associated with IPF through the GeneCards database. Potential targets of pirfenidone were subsequently screened through PubChem and Swiss TargetPrediction, and overlapping targets were identified through Venn diagram analysis. Enrichment analysis of potential target genes was performed to identify the key biological processes and pathways involved in the action of pirfenidone. The main target genes were subsequently identified through the GSE10667 and GSE110147 datasets. The affinity of PDE1A to pirfenidone was predicted by molecular docking and MicroScale Thermophoresis (MST). Finally, the expression and antifibrotic effects of pirfenidone on PDE1A were validated through data from the GSE226249 dataset. PDE1A, identified by GeneCards and Swiss TargetPrediction, was found to be an important mediator of the antifibrotic effect of pirfenidone. The enrichment analysis revealed biological processes such as cyclic nucleotide-mediated signaling and cAMP-mediated signaling. KEGG pathway analysis further linked pirfenidone activity to pathways involved in calcium signaling, taste transduction, morphine dependence, renin secretion and purine metabolism. Molecular docking, molecular dynamics (MD) simulations and MST results revealed a strong binding affinity between pirfenidone and PDE1A. MD simulations showed the stability of the complex. It was observed that the RMSD analysis of the complex stabilized between 0.6 to 0.8 nm throughout the simulation, however RMSF showed minimal fluctuation. Data from the GSE226249 dataset confirmed that upregulation of PDE1A promotes fibrosis, whereas pirfenidone downregulates PDE1A, thereby exerting its antifibrotic effect. The inhibition of IPF progression by pirfenidone is mediated by PDE1A, providing insights into its therapeutic mechanism. - Source: PubMed
Publication date: 2026/04/10
Wu JingKhaliq HaseebKe YanyanUllah QudratSehgal Sheikh ArslanYi Xue - Phosphodiesterase 1A (PDE1A) regulates intracellular cyclic nucleotide signaling and has been implicated in tumor progression, but its clinical relevance and functional role in epithelial ovarian cancer (EOC), particularly in relation to the response to platinum remain unclear. This study aimed to evaluate the clinical significance of PDE1A in EOG and to clarify its functional role in tumor progression and response to platinum-based chemotherapy. - Source: PubMed
Publication date: 2026/02/24
Han Gwan HeeYun HeeChung Joon-YongKim Jae-HoonCho Hanbyoul - - Source: PubMed
Publication date: 2026/02/19
Wang PeiGong Rujun - To explore the effect and mechanism of the Yiqi Huoxue Granule in improving the survival of mesenchymal stem cells (MSCs) induced by hypoxia and promoting angiogenesis in damaged tissues. - Source: PubMed
Publication date: 2026/01/21
Shi WeiliWang ShuhuiLiu ShanshanLei ZhenYan PeishuoWang XinzhouLu ChaoqunQin NanLu Pengfei