INT108422

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Context Info
Confidence 0.36
First Reported 2003
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 11
Total Number 12
Disease Relevance 3.07
Pain Relevance 2.07

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

cytosol (Pde5a) signal transduction (Pde5a)
Anatomy Link Frequency
photoreceptor cells 2
cardiac myocytes 1
brain 1
thalamus 1
heart 1
Pde5a (Mus musculus)
Pain Link Frequency Relevance Heat
agonist 42 99.84 Very High Very High Very High
Morphine 5 98.88 Very High Very High Very High
Thalamus 21 98.28 Very High Very High Very High
adenocard 3 97.46 Very High Very High Very High
Serotonin 77 96.92 Very High Very High Very High
Pain 10 96.68 Very High Very High Very High
Hyperalgesia 1 95.36 Very High Very High Very High
Neurotransmitter 85 90.56 High High
Inflammation 47 88.84 High High
Endocannabinoid 77 88.16 High High
Disease Link Frequency Relevance Heat
Cv General 4 Under Development 46 99.16 Very High Very High Very High
Pain 8 96.68 Very High Very High Very High
Cognitive Disorder 101 96.56 Very High Very High Very High
Hyperalgesia 1 95.36 Very High Very High Very High
Disease 46 95.28 Very High Very High Very High
Nociception 1 92.56 High High
Pulmonary Hypertension 132 89.80 High High
INFLAMMATION 50 88.84 High High
Reprotox - General 2 13 87.84 High High
Hypoxia 8 75.56 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The hypertrophied RV demonstrates increased tissue expression of PDE-5.23 In healthy individuals, PDE-5 is expressed in the coronary arteries, but is not typically found in cardiac myocytes.
PDE-5 Binding (found) of in cardiac myocytes
1) Confidence 0.36 Published 2010 Journal Drug design, development and therapy Section Body Doc Link PMC2880338 Disease Relevance 0.55 Pain Relevance 0
From a historical perspective, PDE inhibitors were used with great caution in heart failure, because the PDE-3 inhibitor milrinone, which increases myocellular cyclic adenosine monophosphate (cAMP) levels, is associated with increased mortality in heart failure.62 However, sildenafil, through its high specificity for PDE-5, is believed to be far safer in this regard.
PDE-5 Binding (specificity) of in heart associated with adenocard and cv general 4 under development
2) Confidence 0.35 Published 2010 Journal Drug design, development and therapy Section Body Doc Link PMC2880338 Disease Relevance 1.05 Pain Relevance 0.05
To date, however, very little is known regarding the potential interaction between selective inhibitors of PDE 3, PDE 4 and PDE 5.
PDE 5 Binding (interaction) of
3) Confidence 0.30 Published 2004 Journal Respir Res Section Body Doc Link PMC419478 Disease Relevance 0.46 Pain Relevance 0.15
The aim of the present study was to investigate the possible peripheral interaction between a PDE-5 inhibitor (sildenafil) and morphine.
PDE-5 Binding (interaction) of associated with morphine
4) Confidence 0.24 Published 2003 Journal Pharmacology Section Abstract Doc Link 12571411 Disease Relevance 0.28 Pain Relevance 0.62
A major source of the NO in these nuclei is in afferent cholinergic fibres, suggesting that presynaptically derived NO is at work whereas the downstream enhancement of excitation was probably postsynaptic, putatively through direct engagement by cGMP of HCN channels that are prominent in the thalamus (Shaw et al., 1999).
cGMP Binding (engagement) of in thalamus associated with thalamus
5) Confidence 0.15 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.21
Binding of cGMP led to the formation of a complex between PKGII and GluR1 and the phosphorylation of GluR1 on a serine residue (serine-845) that facilitates its delivery to extrasynaptic sites, priming insertion into the synapse.
cGMP Binding (Binding) of in synapse
6) Confidence 0.15 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.22
There is also long-standing evidence for an interaction between NO, cGMP and acetylcholine in the brain that remains poorly understood (reviewed by de Vente, 2004).
cGMP Binding (interaction) of in brain
7) Confidence 0.15 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.23
Second messengers cAMP and cGMP
cGMP Binding (messengers) of
8) Confidence 0.14 Published 2008 Journal Psychopharmacology (Berl) Section Body Doc Link PMC2704616 Disease Relevance 0.73 Pain Relevance 0.22
Probably the most widespread mechanism employed by cGMP is activation of PKG, which exists in three forms, PKG1?
cGMP Binding (employed) of
9) Confidence 0.11 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.11
Direct actions of cGMP can be exerted by binding to agonist or regulatory sites on cyclic nucleotide-gated (CNG) ion channels (reviewed in Kaupp & Seifert, 2002) or hyperpolarization-activated, cyclic nucleotide-modulated (HCN) channels (reviewed in Craven & Zagotta, 2006). cGMP also binds directly to the phosphodiesterase (PDE) enzymes PDE2, PDE5 and, in retinal photoreceptor cells, PDE6, resulting in heightened catalytic activity and cGMP breakdown. cGMP is a low-efficacy substrate for another PDE, PDE3, so that cGMP binding to the catalytic site leads to inhibition of cAMP hydrolysis, potentially raising cAMP levels (reviewed by Bender & Beavo, 2006).
cGMP Binding (binding) of in photoreceptor cells associated with agonist
10) Confidence 0.11 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.11
Direct actions of cGMP can be exerted by binding to agonist or regulatory sites on cyclic nucleotide-gated (CNG) ion channels (reviewed in Kaupp & Seifert, 2002) or hyperpolarization-activated, cyclic nucleotide-modulated (HCN) channels (reviewed in Craven & Zagotta, 2006). cGMP also binds directly to the phosphodiesterase (PDE) enzymes PDE2, PDE5 and, in retinal photoreceptor cells, PDE6, resulting in heightened catalytic activity and cGMP breakdown. cGMP is a low-efficacy substrate for another PDE, PDE3, so that cGMP binding to the catalytic site leads to inhibition of cAMP hydrolysis, potentially raising cAMP levels (reviewed by Bender & Beavo, 2006).
cGMP Binding (binding) of in photoreceptor cells associated with agonist
11) Confidence 0.11 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.08
The simulation ignores hydrolysis of cGMP by phosphodiesterases but, at these concentrations, much of the cGMP would probably bind to signalling proteins in the vicinity which would protect it from degradation (Kotera et al., 2003).
cGMP Binding (bind) of
12) Confidence 0.11 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.05

General Comments

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