INT71381

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.79
First Reported 1997
Last Reported 2010
Negated 2
Speculated 3
Reported most in Abstract
Documents 33
Total Number 36
Disease Relevance 11.46
Pain Relevance 8.05

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

cytosol (Nos1) mitochondrion (Nos1) oxidoreductase activity (Nos1)
plasma membrane (Nos1) cytoskeleton (Nos1) nucleus (Nos1)
Anatomy Link Frequency
neuronal 7
spinal cord 3
cerebellum 2
hippocampus 2
synapses 2
Nos1 (Mus musculus)
Pain Link Frequency Relevance Heat
Neuronal nitric oxide synthase 52 100.00 Very High Very High Very High
Pain 50 100.00 Very High Very High Very High
Inflammatory mediators 15 100.00 Very High Very High Very High
cOX1 4 100.00 Very High Very High Very High
COX2 4 100.00 Very High Very High Very High
Spinal cord 93 99.60 Very High Very High Very High
imagery 62 99.32 Very High Very High Very High
Dorsal horn 2 99.24 Very High Very High Very High
metalloproteinase 1 98.62 Very High Very High Very High
Central nervous system 47 98.08 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 231 100.00 Very High Very High Very High
INFLAMMATION 174 100.00 Very High Very High Very High
Increased Venous Pressure Under Development 83 99.68 Very High Very High Very High
Hypersensitivity 181 99.32 Very High Very High Very High
Muscular Dystrophy 256 98.60 Very High Very High Very High
Injury 43 98.56 Very High Very High Very High
Neuropathic Pain 62 98.48 Very High Very High Very High
Nervous System Injury 38 98.28 Very High Very High Very High
Nociception 29 97.12 Very High Very High Very High
Necrosis 20 96.84 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The localization and regulation of neuronal nitric oxide synthase (nNOS), inducible nitric oxide synthase (iNOS) and soluble guanylyl cyclase (sGC) were assessed in the spinal cord of mice stimulated by an intraplantar injection of zymosan.
Localization (localization) of neuronal nitric oxide synthase in spinal cord associated with spinal cord and neuronal nitric oxide synthase
1) Confidence 0.79 Published 2000 Journal Neurosci. Lett. Section Abstract Doc Link 10925177 Disease Relevance 0.14 Pain Relevance 0.18
The localization and regulation of neuronal nitric oxide synthase (nNOS), inducible nitric oxide synthase (iNOS) and soluble guanylyl cyclase (sGC) were assessed in the spinal cord of mice stimulated by an intraplantar injection of zymosan.
Localization (localization) of nNOS in spinal cord associated with spinal cord and neuronal nitric oxide synthase
2) Confidence 0.79 Published 2000 Journal Neurosci. Lett. Section Abstract Doc Link 10925177 Disease Relevance 0.14 Pain Relevance 0.18
In contrast, estradiol caused an increase in IL-10 and NO release by cultured-BAL cells.
Localization (release) of NO
3) Confidence 0.73 Published 2010 Journal Respir Res Section Abstract Doc Link PMC2936382 Disease Relevance 0.81 Pain Relevance 0.11
In a first set of experiments, we assessed the influence of NOS1 or NOS2 deletion in the development and expression of peripheral neuropathic pain.
Localization (deletion) of NOS1 associated with neuropathic pain
4) Confidence 0.71 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3001461 Disease Relevance 0.36 Pain Relevance 0.20
BACKGROUND: The translocation of neuronal nitric oxide synthase (nNOS) from the cytosol to the membrane is functionally coupled to the activation of N-methyl-D-aspartate (NMDA) receptors at synapses.
Localization (translocation) of nNOS in synapses associated with neuronal nitric oxide synthase
5) Confidence 0.70 Published 2009 Journal Molecular pain Section Abstract Doc Link 19619286 Disease Relevance 0.08 Pain Relevance 0.12
Translocation of neuronal nitric oxide synthase to the plasma membrane by ATP is mediated by P2X and P2Y receptors.
Localization (Translocation) of neuronal nitric oxide synthase in neuronal associated with pain and neuronal nitric oxide synthase
6) Confidence 0.70 Published 2009 Journal Molecular pain Section Title Doc Link 19619286 Disease Relevance 0.09 Pain Relevance 0.24
BACKGROUND: The translocation of neuronal nitric oxide synthase (nNOS) from the cytosol to the membrane is functionally coupled to the activation of N-methyl-D-aspartate (NMDA) receptors at synapses.
Localization (translocation) of neuronal nitric oxide synthase in synapses associated with neuronal nitric oxide synthase
7) Confidence 0.70 Published 2009 Journal Molecular pain Section Abstract Doc Link 19619286 Disease Relevance 0.08 Pain Relevance 0.12
Conversely, whereas the P2X receptor antagonist PPADS and the P2Y antagonist reactive blue-2 partially inhibited increases in the translocation of nNOS and [Ca2+]i by ATP, the non-selective P2 receptor antagonist suramin completely blocked them.
Localization (translocation) of nNOS
8) Confidence 0.70 Published 2009 Journal Molecular pain Section Body Doc Link 19619286 Disease Relevance 0 Pain Relevance 0
The purinergic P2X receptor agonist 2-MeSATP and the P2Y agonist UTP significantly enhanced nNOS translocation; and simultaneous stimulation with 2-MeSATP and UTP exhibited the same concentration-response curve for the translocation as obtained with ATP.
Localization (translocation) of nNOS
9) Confidence 0.70 Published 2009 Journal Molecular pain Section Body Doc Link 19619286 Disease Relevance 0 Pain Relevance 0
RESULTS: The translocation of nNOS was induced by ATP in the presence of NMDA and forskolin, an adenylate cyclase activator.
Localization (translocation) of nNOS
10) Confidence 0.70 Published 2009 Journal Molecular pain Section Body Doc Link 19619286 Disease Relevance 0 Pain Relevance 0
We observed that cells collected of BAL and of bone marrow of OVx allergic rats significantly increased the release of inflammatory mediators such as LTB4, NO and TNF-?.
Localization (release) of NO in bone marrow associated with inflammatory mediators and hypersensitivity
11) Confidence 0.68 Published 2010 Journal Respir Res Section Body Doc Link PMC2936382 Disease Relevance 1.13 Pain Relevance 0.18
The present immunohistochemical study details localization and regulation of cyclo-oxygenase-1 and -2 and neuronal nitric oxide synthase in lumbar spinal cord before and after induction of a painful paw inflammation in mice.
Localization (localization) of neuronal nitric oxide synthase in paw associated with pain, inflammation, spinal cord and neuronal nitric oxide synthase
12) Confidence 0.65 Published 2000 Journal Neuroscience Section Abstract Doc Link 11113358 Disease Relevance 0.26 Pain Relevance 0.50
Localization and regulation of cyclo-oxygenase-1 and -2 and neuronal nitric oxide synthase in mouse spinal cord.
Localization (Localization) of neuronal nitric oxide synthase in spinal cord associated with cox1, spinal cord and neuronal nitric oxide synthase
13) Confidence 0.65 Published 2000 Journal Neuroscience Section Title Doc Link 11113358 Disease Relevance 0.25 Pain Relevance 0.82
Cyclo-oxygenase-2 was co-localized with neuronal nitric oxide synthase immunoreactivity in several neurons in superficial laminae of the dorsal horns and in the area surrounding the central canal.
Localization (co-localized) of neuronal nitric oxide synthase in neuronal associated with neuronal nitric oxide synthase
14) Confidence 0.65 Published 2000 Journal Neuroscience Section Abstract Doc Link 11113358 Disease Relevance 0.23 Pain Relevance 0.57
Figures 3a-c demonstrate that, as opposed to wild type mice, the myocardium of nNOS knockout mice could not be protected by the specific NOS inhibitor TRIM as the mean values for CK release and cell necrosis and apoptosis were not significantly different from muscles subjected to ischemia/reoxygenation alone.
Neg (not) Localization (protected) of nNOS in myocardium associated with targeted disruption, necrosis, ischemia and apoptosis
15) Confidence 0.61 Published 2010 Journal BMC Physiol Section Body Doc Link PMC2927582 Disease Relevance 1.35 Pain Relevance 0.11
In addition, the increase in the nNOS translocation by ATP was blocked by NMDA receptor antagonists and inhibitors of protein kinase A, protein kinase C, and Src kinase.
Localization (translocation) of nNOS
16) Confidence 0.61 Published 2009 Journal Molecular pain Section Body Doc Link 19619286 Disease Relevance 0 Pain Relevance 0
We recently established a fluorescence imaging system for examining nNOS translocation in PC12 cells expressing a yellow fluorescence protein-tagged nNOS N-terminal mutant, nNOSNT-YFP, and examined the effect of ATP on nNOS translocation using the system.
Spec (examining) Localization (translocation) of nNOS associated with imagery
17) Confidence 0.61 Published 2009 Journal Molecular pain Section Abstract Doc Link 19619286 Disease Relevance 0.09 Pain Relevance 0.13
Remaining NO-generating capacities in the knock-out mice were demonstrated by immunohistochemical localization of inducible, endothelial and neuronal NOS isoforms.
Localization (localization) of neuronal NOS in neuronal associated with targeted disruption
18) Confidence 0.61 Published 2001 Journal Acta Histochem. Section Abstract Doc Link 11700945 Disease Relevance 0.40 Pain Relevance 0
Intracellularly, cyclo-oxygenase-2 is bound to the membranes of the nucleus and endoplasmic reticulum, whereas neuronal nitric oxide synthase is found in the cytoplasm.
Localization (found) of neuronal nitric oxide synthase in neuronal associated with neuronal nitric oxide synthase
19) Confidence 0.61 Published 2000 Journal Neuroscience Section Abstract Doc Link 11113358 Disease Relevance 0.24 Pain Relevance 0.46
Therefore, we asked whether the current strategy for restoring dystrophin expression increased the level of nNOS protein localized at the myofiber membrane, where it serves to maintain normal cellular function in close association with dystrophin.
Localization (localized) of nNOS protein
20) Confidence 0.59 Published 2008 Journal BMC Biotechnol Section Body Doc Link PMC2362111 Disease Relevance 0 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox