Ask about this productRelated genes to: PDE1C antibody
- Gene:
- PDE1C NIH gene
- Name:
- phosphodiesterase 1C
- Previous symbol:
- -
- Synonyms:
- Hcam3
- Chromosome:
- 7p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-29
- Date modifiied:
- 2016-10-05
Related products to: PDE1C antibody
Related articles to: PDE1C antibody
- Resistance of tumor cells to chemotherapy remains a critical obstacle to effective cancer treatment. Although paclitaxel is one of the most commonly used chemotherapeutic agents for treating triple-negative breast cancer (TNBC), the mechanisms underlying paclitaxel resistance are not fully understood. We previously found that phosphodiesterase 1C (PDE1C) was substantially upregulated in a paclitaxel-resistant T50RN cell clone established from the human TNBC cell line MDA-MD-231. In this study, we aimed to explore whether and how PDE1C modulates resistance to paclitaxel in T50RN cells. Our results showed that depletion of PDE1C enhanced paclitaxel cytotoxicity, and that pharmacological inhibition of PDE1 potentiated paclitaxel-induced antiproliferative and antimitotic effects in T50RN cells. Additionally, intracellular cyclic adenosine monophosphate (cAMP) levels were lower in T50RN cells than in parental MDA-MB-231 cells. PDE1 inhibition restored the cAMP level, suggesting that cAMP-degrading activity of PDE1 is elevated in the T50RN cells. Similar to PDE1 inhibitors, the cell permeable cAMP analog 8‑bromo-cAMP or the adenylate cyclase activator forskolin increased cAMP levels and concurrently augmented paclitaxel-induced cytotoxicity and spindle abnormalities in T50RN cells. Furthermore, PDE1 inhibitors, forskolin, and an agonist of the cAMP downstream effector EPAC enhanced paclitaxel-mediated microtubule (MT) stabilization. Thus, PDE1 inhibition may act through cAMP/EPAC signaling to facilitate MT stabilization and potentiate the antiproliferative and antimitotic effects of paclitaxel in T50RN cells. Upon PDE1 inhibition, paclitaxel-treated T50RN cells exhibited signs of endoplasmic reticulum (ER) stress and apoptosis. Together, our findings indicate that PDE1C overexpression contributes to paclitaxel resistance. - Source: PubMed
Publication date: 2026/04/06
Kuo Hsiao-HuiHuang Chien-WeiLu Tsai-MingChiang Wei-RouYih Ling-Huei - The crosstalk between the hypothalamic-pituitary-gonadal (HPG) and hypothalamic-pituitary-thyroid (HPT) axes plays an important role in gonadal development. However, the mechanism by which these 2 axes regulate early testicular development in drakes remains largely unknown. Therefore, the aim of the present study was to compare the morphology, histology, and transcriptomics between the precocious puberty (PP) and delayed puberty (DP) Longyan Shan-ma drakes (Anas platyrhynchos) to preliminarily reveal the mechanisms regulating early testicular development. - Source: PubMed
Publication date: 2026/01/05
Chen YunyiHu XinyueChi XuliLin YifeiLin RulongChen HongpingCai KaixianChen FenglinYe XiaolongLi XiaopengOuyang QingyuanLi JieZhu LipengLiu HeheHu JiweiLi LiangWang Jiwen - - Source: PubMed
Publication date: 2025/12/29
Zhao YihuanFang KunYang QiandanYan JiawangZhou Yaofeng - Cognitive impairment is a defining feature of neurodegenerative diseases such as Alzheimer's disease (AD) and vascular dementia (VaD). However, the pathogenesis of cognitive impairment remains unclear, mainly because it involves complex pathological processes in which multiple cytokines and pathways contribute to its progression. Among key molecular regulators, cyclic nucleotide phosphodiesterase 1 (PDE1), a Calcium/calmodulin (Ca²⁺/CaM) activated enzyme that regulates intracellular levels of cAMP and cGMP by degrading them to inactive forms. PDE1 may play a critical role in influencing cognitive function through modulating these second messengers. PDE1 integrates calcium fluctuations with cyclic nucleotide metabolism, affecting a series of events including synaptic plasticity, neuronal survival, vascular tone, and neuroinflammatory responses. This review summarizes the distribution of PDE1 and its isoforms, and their regulatory mechanisms and functional roles, particularly those of PDE1A, PDE1B, and PDE1C, in the central nervous system (CNS) disorders. We also discussed the involvement of PDE1 in modulating cAMP/PKA and cGMP/PKG signaling pathways, and its impact on oxidative stress, neuroinflammation, and apoptotic cascades associated with cognitive dysfunction. In addition, this review integrates current evidence on PDE1 isoforms in both neuronal and vascular regulation of cognition, emphasizing their dual neurovascular roles in cognitive impairment. We further summarized recent progress on PDE1 target validation and the reported efficacy of PDE1A inhibitors in alleviating memory deficits associated with neurodegenerative disorders, such as AD and VaD. - Source: PubMed
Publication date: 2025/11/21
Li HailiangBrzostek OliviaSherman JasonAyoub MathewChen LingSheng ZhutaoXu FuDou BaominWang WeizhengZhu XiongweiYan ChenXu Ying - The phosphodiesterase 1 genes PDE1A, PDE1B, and PDE1C encode calcium-regulated cyclic nucleotide phosphodiesterases that mediate the interplay between calcium and cyclic nucleotide signaling in the brain, heart, and vasculature. While an inhibitory domain and a calmodulin-binding domain have been identified in PDE1, the mechanism of regulation is not understood. In this study, we investigated the regulatory mechanism through a series of experiments. The experimental data, supported by AlphaFold structure predictions, consistently point to the following model of PDE1 regulation: In the absence of calcium, the inhibitory domain of PDE1 binds to and blocks the catalytic site via molecular interactions that closely resemble those observed in autoinhibited PDE4. Upon calcium/calmodulin binding to PDE1's calmodulin-binding domain, steric constraints prevent the inhibitory domain from reaching the catalytic site, thereby activating PDE1. Understanding this mode of PDE1 regulation may open new avenues for pharmacological intervention. Moreover, it establishes PDE1 and PDE4 as a second mechanistic class of phosphodiesterase regulation in addition to the GAF-domain-mediated regulation known to control the activity of several other PDEs. - Source: PubMed
Publication date: 2025/11/01
Nielsen JacobLanggård MortenTengberg Josefine FussingKehler Jan