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PDE3A is downregulated in chemoresistant NSCLC cells due to DNA hypermethylation.
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Vulnerability to antineoplastic phosphodiesterase inhibitors inhibitors has been associated with co-expression of PDE3A and SLFN12 in various tumor types.
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We found a novel heterozygous missense mutation c.1336T>C in exon 4 of the PDE3A gene in a Japanese family with multiple HTNB patients. This mutation was found to be completely linked to the family members who inherited this condition.
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The genetic variant, rs3794271, located within the PDE3A-SLCO1C1 locus was analyzed for correlation with treatment response using both the EULAR classification criteria and absolute change in (Delta)DAS28 scores as outcome measures correlated with anti-TNF response in a large UK rheumatoid arthritis cohort.
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PDE3A is a low-affinity and high-velocity enzyme for hydrolysis of cUMP in cardiac myocytes.
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Chemical proteomics results show that besides known interactors such as 14-3-3 family proteins, PDE3A was found to associate with a PP2A complex composed of a regulatory, scaffold and catalytic subunit.
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We found a highly significant association between PDE3A-SLCO1C1 and the clinical response to TNF blockers
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Epigenetic regulation of phosphodiesterases 2A and 3A underlies compromised beta-adrenergic Signaling in an induced pluripotent stem cell model of dilated cardiomyopathy.
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A heterozygous missense mutation in PDE3A causes autosomal dominant hypertension with brachydactyly.
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PDE3A is part of a SERCA2 signaling complex in cardiac myocytes.
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the genotypic and allelic frequencies of the rs7134375 SNP are different between the Mulao and Han populations. the PDE3A rs7134375 SNP is associated with serum TG levels in the Mulao population, however, not in the Han population.
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The PDE3A-SLCO1C1 locus rs3794271 SNP showed a highly significant association with anti-TNF treatment response.
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PI3Kgamma coordinates the coincident signaling of the major cardiac PDE3 and PDE4 isoforms, thus orchestrating a feedback loop that prevents calcium-dependent ventricular arrhythmia.
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Anagrelide suppresses megakaryocytopoiesis by reducing the expression levels of GATA-1 and FOG-1 via a PDEIII-independent mechanism that is differentiation context-specific and does not involve inhibition of MPL-mediated early signal transduction events
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Data show that PDE3A inhibition augments CFTR-dependent submucosal gland secretion and actin skeleton disruption decreases secretion.
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There was a concentration-dependent inhibition in the increase of intracellular Ca2+ with PDE3 inhibition and significantly less with PDE2 inhibition.
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These findings suggest that alternative processing of the PDE3A gene results in the generation of two mRNAs and three protein isoforms in cardiac myocytes that differ in intracellular localization and may be regulated through different signaling pathways.
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PDE3A gene transcript levels are increased in the intrapulmonary and resistance pulmonary arteries by chronic hypoxia.
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Presence of phosphodiesterase type 3 A (PDE 3A) mRNA was confirmed in human germinal vesicle-stage (GV) oocytes. A selective PDE 3 inhibitor, Org 9935, arrested oocytes retrieved from immature follicles in prophase I for up to 72 h.
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PDE3, but not of PDE5, extends to all major processes in thrombus formation: assembly of platelets into aggregates, secretion of autocrine products, and procoagulant activity.
