Ask about this productRelated genes to: PDE3A antibody
- Gene:
- PDE3A NIH gene
- Name:
- phosphodiesterase 3A
- Previous symbol:
- -
- Synonyms:
- CGI-PDE
- Chromosome:
- 12p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-29
- Date modifiied:
- 2018-07-11
Related products to: PDE3A antibody
Related articles to: PDE3A antibody
- Quercetin is an abundant dietary flavonol with interesting properties that include substrate-selective positive allosteric modulation (PAM) of the activity of the receptor type protein tyrosine phosphatase D (PTPRD) and substantial antioxidant actions. Its activities include reducing incidence of Alzheimer's disease (AD) and reducing AD neurofibrillary pathology in mouse models. Structure-activity studies have identified quercetin analogs with improved and properties, including the improved PTPRD PAM 6-bromoquercetin (6BrQ). However, there is no comparison of the antioxidant properties of 6BrQ to those of quercetin. There is no systematic screening for activities of quercetin or of 6BrQ using a panel of targets for most currently-used drugs. We now report that both quercetin and 6BrQ provide equivalent results in cyclic voltammetric and biochemical antioxidant assays. We also report that neither 10 M quercetin nor 6BrQ provides any significant (>50%) effects on any of the 104 assays in a Eurofins off-target screening panel. At 10 M, both quercetin and 6BrQ exert significant effects in assays for glycogen synthase kinase 3 (GSK3β) as well as those for serotonin 5HT2B receptor, adenosine transport, adenosine A2A receptors, cyclooxygenases COX1 and COX2, phosphodiesterases PDE3A and 4D2 and PPAR gamma. These data extend prior characterization of quercetin's biochemical effects, provide novel results for 6BrQ and support the likelihood that both quercetin and 6BrQ can a) directly inhibit GSK3, b) reduce GSK3 activities enhancement of its dephosphorylation by PTPRD and c) display modest numbers of off target activities at high concentrations, several of which could conceivably contribute to anti-AD activities. These results advance bioavailable glycosylated prodrugs that can be metabolized to 6BrQ as developmental candidates for AD. - Source: PubMed
Publication date: 2026/03/13
Uhl George RKannan BalajiHess EmilyHenderson Schultz Kevin - The cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling pathway plays a central role in adrenal function, steroidogenesis, and blood pressure regulation. Increasing evidence suggests that dysregulation of this pathway contributes to several forms of hypertension, both endocrine and non-endocrine. A growing number of germline and somatic alterations affecting components of the cAMP/PKA axis have been implicated as key drivers of hypertensive disorders. Among these, activating pathogenic variants (PV) in , which encodes the stimulatory G protein α-subunit (Gsα) responsible for cAMP production, have been linked to cortisol excess. Mosaic PV , which may present with ACTH-independent Cushing syndrome, while somatic PV have been identified in cortisol-producing adrenal adenomas. Germline inactivating variants in are associated with Furthermore, germline alterations in phosphodiesterases such as and , which impair cAMP degradation, have been associated with Cushing syndrome and micronodular adrenal hyperplasia. Somatic activating PV in , the gene encoding the catalytic subunit of PKA, have also been described in cortisol-producing adenomas. In primary aldosteronism, recent studies-including data from our group-suggest that germline variants in and may contribute to bilateral adrenal hyperplasia and autonomous aldosterone production by modulating intracellular cAMP levels. Additionally, gain-of-function PV in have been associated with a familial form of salt-independent hypertension characterized by enhanced PKA signaling and vascular remodeling. This expanding body of evidence underscores the critical role of the cAMP/PKA pathway in the pathophysiology of distinct hypertensive phenotypes and highlights novel molecular mechanisms and potential therapeutic targets that merit further investigation. - Source: PubMed
Publication date: 2026/02/24
Lima Sobrinho Jose Antonio BAlmeida Madson Q - Left and right ventricular imaging measures are essential for heart failure diagnosis and prognostication, yet their genetic architecture remains underexplored. We conduct genome-wide association analyses of twenty left and right cardiovascular magnetic resonance phenotypes in 56,509 UK Biobank participants, including conventional measurements (e.g., volumes/ejection fraction) and novel parameters (left ventricular global function index and myocardial contraction fraction). We identify 200 loci associated with at least one phenotype (P < 5×10); 58 being novel. A polygenic risk score for left ventricular global function index negative associates with heart failure in phenome-wide scan. Rare variant analysis reveals enrichment of deleterious variants across 13 genes (P < 2.5×10). Colocalisation with heart failure implicates 23 shared loci and bioinformatic analysis prioritises genes including HSPB7, CAMK2D, ALDH2, ENG, and YWHAE. Druggability analysis highlights PDE3A, informing divergent effects of non-selective PDE3 inhibition. In this work, we expand our knowledge of cardiac ventricular genetics, suggesting potential heart failure therapeutic targets. - Source: PubMed
Publication date: 2026/02/27
Nicholls Hannah LVargas Jose DSanghvi Mihir MAhn Hyo-SukChahal C Anwar AKhanji Mohammed YPetersen Steffen EMunroe Patricia BAung Nay - PDE3A is a key member of the cyclic nucleotide phosphodiesterase family. By modulating intracellular cAMP and cGMP levels, it participates in diverse physiological processes such as platelet activation, cardiac function, oocyte maturation, and vascular smooth muscle cell proliferation. Recent studies have revealed that PDE3A also plays critical roles in multiple malignant tumors. This study aims to investigate the regulation of PDE3A expression, its role in cancer, and its potential as a therapeutic target, with a particular focus on its impact on tumor cell proliferation, metastasis, and resistance to chemotherapy. - Source: PubMed
Publication date: 2026/02/05
Pu ShengyuZhang QiheMiao MiChen BohongXu JiaruiLei JingyiTang XiaojiangHao Na - Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder with a detrimental effect on reproductive outcomes due to compromised oocyte quality. The exact mechanism of hyperandrogen-induced anovulation in PCOS is largely unknown to date. The maintenance of oocyte meiotic arrest is primarily attributed to high cytoplasmic concentrations of cyclic adenosine monophosphate (cAMP), which is hydrolyzed by . - Source: PubMed
Publication date: 2026/02/11
Pei ZhenleDeng KeCao HaifengDing ZiyinXu CongjianZhang Shuo