INT276027

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Context Info
Confidence 0.59
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 7
Disease Relevance 0.71
Pain Relevance 0.32

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

signal transduction (Pde1b) nucleus (Pde1b) cytoplasm (Pde1b)
Pde1b (Mus musculus)
Pain Link Frequency Relevance Heat
Glutamate receptor 6 91.52 High High
Serotonin 6 89.60 High High
dopamine receptor 6 89.16 High High
Pyramidal cell 6 78.28 Quite High
depression 54 64.96 Quite High
Bioavailability 1 57.28 Quite High
gABA 66 56.76 Quite High
Kinase C 6 39.20 Quite Low
imagery 30 5.00 Very Low Very Low Very Low
long-term potentiation 24 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Disease 17 99.68 Very High Very High Very High
Pulmonary Hypertension 66 99.22 Very High Very High Very High
Apoptosis 2 84.56 Quite High
Depression 54 64.96 Quite High
Hypoxia 4 44.96 Quite Low
Renal Insufficiency 1 32.32 Quite Low
Cirrhosis 1 19.52 Low Low
Increased Venous Pressure Under Development 5 6.00 Low Low
Cv General 4 Under Development 22 5.00 Very Low Very Low Very Low
Adhesions 12 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
On the other hand, a PDE1 increase of >30% made it impossible for any increase of [Ca2+]i (up to 10 ?
Positive_regulation (increase) of PDE1
1) Confidence 0.59 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
One is Ca2+/CaM-activated PDE1, which breaks down both cAMP and cGMP (Polli and Kincaid, 1994).
Positive_regulation (activated) of PDE1
2) Confidence 0.43 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0.18 Pain Relevance 0.26
This study clarified that Ca2+/CaM-activated PDE1 constitutes a feedforward inhibitory pathway and controls the [Ca2+]i threshold by suppressing the CaMKII activity through cAMP, PKA, DARPP-32, and PP-1.
Positive_regulation (activated) of PDE1
3) Confidence 0.43 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Thus, the amounts of cAMP and active PKA were transiently decreased by PDE1 activation during the [Ca2+]i increase, and then showed a sustained increase after the end of the [Ca2+]i increase (Figure 2G and H).
Positive_regulation (activation) of PDE1
4) Confidence 0.43 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.03
The PKA activity seems to be regulated by the activity of PDE1 in the basal condition owing to the high affinity of PDE1 for Ca2+/CaM (Kd ?
Positive_regulation (activity) of PDE1
5) Confidence 0.43 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
In the absence of PDE1, the [Ca2+]i increase required for triggering sustained CaMKII activation (>1 ?
Positive_regulation (absence) of PDE1
6) Confidence 0.43 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
One study comparing sildenafil to inhaled NO (iNO) demonstrated comparable reductions in PA pressures and pulmonary vascular resistance (PVR), but increased cardiac index (CI) was seen only with sildenafil treatment, consistent with an inotropic effect.24 However, other investigators, examining load-independent measures of myocardial performance, found no changes in systolic or diastolic function with sildenafil treatment.25 Circulating endothelial progenitor cells are reduced in idiopathic PAH and congenital PAH, and treatment with sildenafil has been shown to increase these cells to levels consistently higher than other PAH therapies.26 Sildenafil also inhibits PDE-1, which is expressed in low levels in the pulmonary circulation under baseline conditions but is upregulated in the disease state.27 The clinical significance of these findings remains uncertain.
Positive_regulation (upregulated) of PDE-1 associated with pulmonary hypertension and disease
7) Confidence 0.11 Published 2010 Journal Drug design, development and therapy Section Body Doc Link PMC2880338 Disease Relevance 0.54 Pain Relevance 0.03

General Comments

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