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anti-Mouse (Murine) PDE3A Anticorps:
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Human Polyclonal PDE3A Primary Antibody pour ELISA, IHC - ABIN2747088
Uckert, Hedlund, Waldkirch, Sohn, Jonas, Andersson, Stief: Interactions between cGMP- and cAMP-pathways are involved in the regulation of penile smooth muscle tone. dans World journal of urology 2005
Show all 18 Pubmed References
Human Polyclonal PDE3A Primary Antibody pour IP, ELISA - ABIN2747090
Macdougall, Agarwal, Stopford, Chu, Collins, Longster, Colyer, Harvey, Calaghan: Caveolae compartmentalise β2-adrenoceptor signals by curtailing cAMP production and maintaining phosphatase activity in the sarcoplasmic reticulum of the adult ventricular myocyte. dans Journal of molecular and cellular cardiology 2012
Study demonstrated the presence of PDE3 protein and mRNA in human and murine airway tissues and concluded that PDE3A or PDE3B deficiency or pharmacological inhibition of PDE3 may alleviate the symptoms of allergic airway inflammation in a house dust mite-driven allergic airway inflammation mouse model.
NO-GC modulates PDE3A expression.
Data show that phosphodiesterase 3A (PDE3A) was expressed throughout interstitial cells of Cajal (ICC) development and that ICC density was halved in PDE3A-deficient mice.
PDE3A is a low-affinity and high-velocity enzyme for hydrolysis of cUMP in cardiac myocytes.
These together indicate that PDE3A1 negatively regulates beta-AR signaling and protects against I/R injury by inhibiting cardiomyocyte apoptosis.
PDE3A is the primary isozyme modulating basal myocardial contractility and sarcoplasmic reticulum divalent calcium ion (Ca2+) content.
Discussion of role of PDE3A, not PDE3B, in cell cycle progression in vascular smooth muscle and oocytes via regulation of cAMP levels. Is inhibition of PDE3A a possible target for treatment of cardiovascular diseases or female infertility? [REVIEW]
PDE3A regulates VSMC growth via two complementary pathways
phosphodiesterase-III inhibitor prevents the hemorrhagic transformation induced by focal cerebral ischemia in mice treated with tPA
Results provide evidence indicating that resumption of meiosis in vivo and in vitro requires cyclic nucleotide phosphodiesterase 3A activity.
These data indicate that activation of PDE3A by PKB/Akt-mediated phosphorylation plays a role in the control of PDE3A activity in mammalian oocytes.
Role of Pde3a in regulating platelet and cardiac function using subtype-selective knockout mice is reported.
Gpr3 is epistatic to Pde3a and fertility as well as meiotic arrest in the PDE3A-deficient oocyte is dependent on the activity of GPR3.
PDE3A is downregulated in chemoresistant NSCLC cells due to DNA hypermethylation.
Vulnerability to antineoplastic phosphodiesterase inhibitors inhibitors has been associated with co-expression of PDE3A and SLFN12 in various tumor types.
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.
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.
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.
We found a highly significant association between PDE3A-SLCO1C1 and the clinical response to TNF blockers
Epigenetic regulation of phosphodiesterases 2A and 3A underlies compromised beta-adrenergic Signaling in an induced pluripotent stem cell model of dilated cardiomyopathy.
A heterozygous missense mutation in PDE3A causes autosomal dominant hypertension with brachydactyly.
PDE3A is part of a SERCA2 signaling complex in cardiac myocytes.
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.
The PDE3A-SLCO1C1 locus rs3794271 SNP showed a highly significant association with anti-TNF treatment response.
PI3Kgamma coordinates the coincident signaling of the major cardiac PDE3 and PDE4 isoforms, thus orchestrating a feedback loop that prevents calcium-dependent ventricular arrhythmia.
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
Data show that PDE3A inhibition augments CFTR-dependent submucosal gland secretion and actin skeleton disruption decreases secretion.
There was a concentration-dependent inhibition in the increase of intracellular Ca2+ with PDE3 inhibition and significantly less with PDE2 inhibition.
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.
PDE3A gene transcript levels are increased in the intrapulmonary and resistance pulmonary arteries by chronic hypoxia.
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.
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.
Results demonstrated that PDE3A is the major cAMP-degrading PDE in the oocyte.
Degradation of the intracellular cyclic nucleotide by Pde3a is transcriptionally up-regulated via a cAMP-dependent pathway in cumulus cells, suggesting that it has a functional role during the ovulatory gonadotropin surge.
This gene encodes a member of the cGMP-inhibited cyclic nucleotide phosphodiesterase (cGI-PDE) family. cGI-PDE enzymes hydrolyze both cAMP and cGMP, and play critical roles in many cellular processes by regulating the amplitude and duration of intracellular cyclic nucleotide signals. The encoded protein mediates platelet aggregation and also plays important roles in cardiovascular function by regulating vascular smooth muscle contraction and relaxation. Inhibitors of the encoded protein may be effective in treating congestive heart failure. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
phosphodiesterase 3A, cGMP-inhibited
, cGMP-inhibited 3',5'-cyclic phosphodiesterase A
, phosphodiesterase 3a
, cGMP-inhibited 3',5'-cyclic phosphodiesterase A-like
, CGI-PDE A
, cGMP-inhibited phosphodiesterase
, cyclic GMP-inhibited phosphodiesterase A
, cyclic nucleotide phosphodiesterase
, cAMP phosphodiesterase, myocardial cGMP-inhibited