INT94861

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.69
First Reported 2001
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 40
Total Number 40
Disease Relevance 14.73
Pain Relevance 13.27

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
neuronal 3
ganglia 3
liver 2
myocytes 2
dorsal root ganglia 2
Pde5a (Rattus norvegicus)
Pain Link Frequency Relevance Heat
amygdala 147 100.00 Very High Very High Very High
antinociception 66 99.96 Very High Very High Very High
trigeminal ganglion 28 99.92 Very High Very High Very High
bradykinin 7 99.84 Very High Very High Very High
qutenza 14 99.56 Very High Very High Very High
analgesia 4 99.52 Very High Very High Very High
dorsal root ganglion 23 99.04 Very High Very High Very High
Hyperalgesia 42 98.40 Very High Very High Very High
Antinociceptive 36 97.12 Very High Very High Very High
gABA 44 96.40 Very High Very High Very High
Disease Link Frequency Relevance Heat
Ganglion Cysts 58 99.92 Very High Very High Very High
Cirrhosis 5 98.84 Very High Very High Very High
Hyperalgesia 48 98.40 Very High Very High Very High
Anxiety Disorder 79 97.76 Very High Very High Very High
Nociception 30 96.84 Very High Very High Very High
Headache 49 96.00 Very High Very High Very High
Neuropathic Pain 142 95.58 Very High Very High Very High
Nicotine Addiction 34 91.36 High High
Overweight 1 91.00 High High
Increased Venous Pressure Under Development 69 89.12 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In conclusion, PDE3A, PDE3B, PDE5A, and five CNG subunits were expressed in several components of the trigeminovascular system of the rat.
Gene_expression (expressed) of PDE5A
1) Confidence 0.69 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16808996 Disease Relevance 0.49 Pain Relevance 0.58
PDE5A and PDE3A protein expression was present in both cerebral and peripheral arteries, whereas PDE3B protein was present only in the cerebral arteries.
Gene_expression (expression) of PDE5A
2) Confidence 0.69 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16808996 Disease Relevance 0.69 Pain Relevance 0.57
The aim of the present study was to describe the expression of phosphodiesterase 3 (PDE3) and 5 (PDE5) and cyclic nucleotide-gated ion channels (CNG) in cerebral arteries, meninges, and the trigeminal ganglion. mRNA for PDE and CNG was determined in the rat middle cerebral artery, basilar artery, trigeminal ganglion, and dura mater using real-time PCR.
Gene_expression (expression) of PDE5 in basilar artery associated with ganglion cysts and trigeminal ganglion
3) Confidence 0.60 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16808996 Disease Relevance 0.71 Pain Relevance 0.58
PDE5A and PDE3A protein expression was present in both cerebral and peripheral arteries, whereas PDE3B protein was present only in the cerebral arteries.
Gene_expression (expression) of PDE5A
4) Confidence 0.60 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16808996 Disease Relevance 0.69 Pain Relevance 0.57
Previous studies demonstrated increased phosphodiesterase-5 (PDE5) activity and expression in the kidneys of rats with liver cirrhosis.
Gene_expression (expression) of PDE5 in liver associated with cirrhosis
5) Confidence 0.54 Published 2007 Journal Eur. J. Pharmacol. Section Abstract Doc Link 17610866 Disease Relevance 0.31 Pain Relevance 0.04
Due to its peculiar chemical and pharmacokinetics properties (essentially half-life), tadalafil may be considered as the least “typical” among the current generation of PDE5 inhibitors (Montorsi et al 2004).
Gene_expression (generation) of PDE5
6) Confidence 0.44 Published 2006 Journal Clinical Interventions in Aging Section Body Doc Link PMC2699638 Disease Relevance 0.73 Pain Relevance 0.05
NO passively crosses the cell membrane and activates soluble guanylyl cyclase (sGC) upon entering smooth muscle cytoplasm, which in turn increases the production of cyclic guanosine monophosphate (cGMP) by converting it from guanosine triphosphate (GTP) (Lincoln and Cornwell 1991).
Gene_expression (production) of cGMP in smooth muscle
7) Confidence 0.31 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2643112 Disease Relevance 0.13 Pain Relevance 0.20
This proposal was based on the observation that local injection of dibutyryl-cGMP produced antinociception in a modification of the Randall-Selitto hyperalgesia (3).
Gene_expression (produced) of cGMP associated with antinociception and hyperalgesia
8) Confidence 0.28 Published 2008 Journal Journal of Korean Medical Science Section Body Doc Link PMC2610640 Disease Relevance 0.54 Pain Relevance 0.79
Rat clitorises express components of the proposed pathway: neuronal and endothelial NO synthases, soluble guanylyl cyclase (sGC), type 5 phosphodiesterase (PDE-5), and BK(Ca) channels.
Gene_expression (express) of PDE-5 in neuronal
9) Confidence 0.26 Published 2004 Journal FASEB J. Section Abstract Doc Link 15333581 Disease Relevance 0.17 Pain Relevance 0.23
Guanylyl cyclase catalyzes the formation of cGMP from GTP, leading to the synthesis of cGMP, whereas cGMP-specific phosphodiesterase catalyzes the hydrolysis of cGMP to GMP, thereby ending signal transduction (5).
Gene_expression (synthesis) of cGMP
10) Confidence 0.25 Published 2008 Journal Journal of Korean Medical Science Section Body Doc Link PMC2610640 Disease Relevance 0.53 Pain Relevance 0.53
PDE1A1, PDE1A4, and PDE1A8 have the N2 terminal sequence and are widely expressed in lung and other tissues, whilst PDE1A5, PDE1A6, and PDE1A9 have the N1 sequence and are expressed in brain tissue and PDE1A10 and PDE1A11 which have the N3 sequence are expressed in testis (Michibata et al 2001).
Gene_expression (expressed) of PDE1A5 in testis
11) Confidence 0.24 Published 2008 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2650605 Disease Relevance 0 Pain Relevance 0
The aim of the present study was to describe the expression of phosphodiesterase 3 (PDE3) and 5 (PDE5) and cyclic nucleotide-gated ion channels (CNG) in cerebral arteries, meninges, and the trigeminal ganglion. mRNA for PDE and CNG was determined in the rat middle cerebral artery, basilar artery, trigeminal ganglion, and dura mater using real-time PCR.
Gene_expression (expression) of PDE5 in trigeminal ganglion associated with ganglion cysts and trigeminal ganglion
12) Confidence 0.20 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16808996 Disease Relevance 0.71 Pain Relevance 0.58
The aim of the present study was to describe the expression of phosphodiesterase 3 (PDE3) and 5 (PDE5) and cyclic nucleotide-gated ion channels (CNG) in cerebral arteries, meninges, and the trigeminal ganglion. mRNA for PDE and CNG was determined in the rat middle cerebral artery, basilar artery, trigeminal ganglion, and dura mater using real-time PCR.
Gene_expression (expression) of PDE5 in dura mater associated with ganglion cysts and trigeminal ganglion
13) Confidence 0.20 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16808996 Disease Relevance 0.71 Pain Relevance 0.58
The aim of the present study was to describe the expression of phosphodiesterase 3 (PDE3) and 5 (PDE5) and cyclic nucleotide-gated ion channels (CNG) in cerebral arteries, meninges, and the trigeminal ganglion. mRNA for PDE and CNG was determined in the rat middle cerebral artery, basilar artery, trigeminal ganglion, and dura mater using real-time PCR.
Gene_expression (expression) of PDE5 in middle cerebral artery associated with ganglion cysts and trigeminal ganglion
14) Confidence 0.20 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16808996 Disease Relevance 0.71 Pain Relevance 0.58
Guanylyl cyclase catalyzes the formation of cyclic guanosine monophosphate (cGMP) from GTP, leading to the synthesis of cGMP, whereas cGMP-specific phosphodiesterase catalyzes the hydrolysis of cGMP to GMP.2 Accordingly, intracellular cGMP concentrations are regulated by the action of guanylyl cyclase and the rate of degradation by cGMP-specific phosphodiesterase.6,7
Gene_expression (synthesis) of cGMP
15) Confidence 0.18 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2799976 Disease Relevance 1.14 Pain Relevance 1.40
PDE5A1 and A2 isoforms are expressed in a wide variety of tissues, including lung, heart, skeletal muscle, brain, kidney, and liver, but the A3 isoform is confined to tissues with a smooth muscle or cardiac muscle component (Lin et al 2000).
Gene_expression (expressed) of PDE5A1 in brain
16) Confidence 0.18 Published 2008 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2650605 Disease Relevance 0.22 Pain Relevance 0.07
The regulatory domains include the calmodulin binding domain found in PDE1, the cGMP binding (GAF) domains found in PDE2, 5, 6, 10, and 11, and the so called upstream conserved regions 1 and 2 (UCR1 and UCR2) found in PDE4.
Gene_expression (binding) of cGMP
17) Confidence 0.18 Published 2008 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2650605 Disease Relevance 0 Pain Relevance 0
PDE4 is not inhibited by cGMP and thus originally PDE3 was called cGMP-inhibited PDE to distinguish it from PDE4. cGMP inhibition of PDE3 may be physiologically relevant to the elevation of cAMP levels in a variety of cells including human myocytes, where nitric oxide induced relaxation may be mediated by activation of guanylyl cyclase, elevation of intracellular cGMP levels and inhibition of PDE3 leading to elevated cAMP levels (Kirstein et al 1995).
Gene_expression (elevation) of cGMP in myocytes
18) Confidence 0.18 Published 2008 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2650605 Disease Relevance 0.19 Pain Relevance 0.03
PDE4 is not inhibited by cGMP and thus originally PDE3 was called cGMP-inhibited PDE to distinguish it from PDE4. cGMP inhibition of PDE3 may be physiologically relevant to the elevation of cAMP levels in a variety of cells including human myocytes, where nitric oxide induced relaxation may be mediated by activation of guanylyl cyclase, elevation of intracellular cGMP levels and inhibition of PDE3 leading to elevated cAMP levels (Kirstein et al 1995).
Gene_expression (levels) of cGMP in myocytes
19) Confidence 0.18 Published 2008 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2650605 Disease Relevance 0.19 Pain Relevance 0.03
In most cells and tissues, the capacity for hydrolysis of cyclic nucleotides by PDEs is an order of magnitude greater than the maximum rate of synthesis of cAMP and cGMP and thus small reductions in the activity of PDEs can produce large increases in the level of cyclic nucleotides and significant changes in the activity of cAMP-dependent protein kinase.
Gene_expression (synthesis) of cGMP
20) Confidence 0.16 Published 2008 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2650605 Disease Relevance 0.32 Pain Relevance 0.04

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox