INT128746

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Context Info
Confidence 0.52
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 11
Total Number 15
Disease Relevance 8.43
Pain Relevance 4.61

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

cytosol (Gsk3a) signal transduction (Gsk3a) carbohydrate metabolic process (Gsk3a)
Anatomy Link Frequency
neurons 2
hippocampus 1
Gsk3a (Rattus norvegicus)
Pain Link Frequency Relevance Heat
addiction 8 99.92 Very High Very High Very High
Hyperalgesia 7 99.56 Very High Very High Very High
Hippocampus 32 99.28 Very High Very High Very High
intrathecal 2 99.28 Very High Very High Very High
bDMF 80 99.08 Very High Very High Very High
Nerve growth factor 6 98.72 Very High Very High Very High
Morphine 12 98.70 Very High Very High Very High
Kinase C 6 97.80 Very High Very High Very High
tail-flick 1 96.04 Very High Very High Very High
Analgesic 4 94.52 High High
Disease Link Frequency Relevance Heat
Apoptosis 86 100.00 Very High Very High Very High
Hyperalgesia 7 99.56 Very High Very High Very High
Neurodegenerative Disease 38 99.20 Very High Very High Very High
Brain Injury 114 97.48 Very High Very High Very High
Injury 116 96.24 Very High Very High Very High
Edema 10 94.12 High High
Cognitive Disorder 40 93.24 High High
Death 33 87.64 High High
Shock 7 85.76 High High
Pancreatic Cancer 34 85.52 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
When injections of morphine were preceded by intrathecal (i.t.) administration of either an inhibitor of GSK3 [(3-(2,4-dichlorophenyl)-4-(1-methyl-1H-indol-3-yl)-1H-pyrrole-2,5-dione (SB216763) or 6-bromoindirubin-3'oxime] or an inhibitor of cyclin-dependent kinase (Cdk), roscovitine, development of tolerance to morphine analgesia was completely abolished.
Negative_regulation (inhibitor) of GSK3 associated with tolerance, analgesia, intrathecal and morphine
1) Confidence 0.52 Published 2006 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 16902054 Disease Relevance 0 Pain Relevance 1.55
Dose-response studies revealed that systemic administration of 400 mg/kg (i.p.), but not 15, 30, 60 or 100 mg/kg, increases histone H3 and H4 acetylation, and reduces GSK-3 activity, in the hippocampus.
Negative_regulation (reduces) of GSK-3 in hippocampus associated with hippocampus
2) Confidence 0.34 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2894851 Disease Relevance 1.14 Pain Relevance 0.19
Consistent with its dose response to inhibit GSK-3 and HDACs, valproate at 400 mg/kg, but not 100 mg/kg, reduced TBI-associated hippocampal dendritic damage, lessened cortical contusion volume, and improved motor function and spatial memory.
Negative_regulation (inhibit) of GSK-3 associated with brain injury
3) Confidence 0.25 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2894851 Disease Relevance 1.12 Pain Relevance 0.17
Although inhibitors of kinases downstream of PI3K and PLCgamma[glycogen synthetase kinase 3 (GSK3), calmodulin-dependent protein kinase II (CAMII-K) or protein kinase C (PKC)] do not reduce mechanical hyperalgesia, hyperalgesia induced by activation of PI3K was blocked by ERK/MEK inhibitors, suggesting cross-talk from the PI3K to the ERK/MEK signalling pathway.
Negative_regulation (inhibitors) of GSK3 associated with hyperalgesia and kinase c
4) Confidence 0.12 Published 2005 Journal Eur. J. Neurosci. Section Abstract Doc Link 16026476 Disease Relevance 0.60 Pain Relevance 1.16
Figure 5 show that pre-treatment with the PKC inhibitor Gö 6976 did not alter the loss in GSK3 phosphorylation levels induced by the PI3K inhibitor, but totally prevented the recovery mediated by BzATP, NMDA and BDNF.
Negative_regulation (loss) of GSK3
5) Confidence 0.12 Published 2010 Journal Cell Mol Life Sci Section Body Doc Link PMC2858808 Disease Relevance 0.08 Pain Relevance 0
In this context, several treatments capable of rescuing granule neurons from low-potassium induced apoptosis, such as high potassium, IGF-I and cAMP, were described to converge on GSK3 inhibition [17].
Negative_regulation (inhibition) of GSK3 in neurons associated with apoptosis
6) Confidence 0.09 Published 2010 Journal Cell Mol Life Sci Section Body Doc Link PMC2858808 Disease Relevance 0.80 Pain Relevance 0.07
To substantiate the calcium dependence of GSK3 inhibition displayed by the effectors, other strategies were tested.
Negative_regulation (inhibition) of GSK3 associated with addiction
7) Confidence 0.09 Published 2010 Journal Cell Mol Life Sci Section Body Doc Link PMC2858808 Disease Relevance 0 Pain Relevance 0.11
In addition, GSK3 cooperates and contributes to apoptotic signalling, such as JNK activation, during trophic deprivation [16].
Negative_regulation (deprivation) of GSK3 associated with apoptosis
8) Confidence 0.09 Published 2010 Journal Cell Mol Life Sci Section Body Doc Link PMC2858808 Disease Relevance 0.81 Pain Relevance 0.07
It has been reported that lithium inhibition of GSK-3?
Negative_regulation (inhibition) of GSK-3
9) Confidence 0.05 Published 2010 Journal Human Genomics and Proteomics : HGP Section Body Doc Link PMC2958627 Disease Relevance 0.28 Pain Relevance 0.17
A recent finding from a gene expression study performed on cultured rat cortical neurons showed that the treatment with lithium or VPA induced activation of the promoter IV of BDNF and that this activation was mediated by the inhibition of GSK-3 and HDAC, respectively [122].
Negative_regulation (inhibition) of GSK-3 in neurons associated with bdmf
10) Confidence 0.04 Published 2010 Journal Human Genomics and Proteomics : HGP Section Body Doc Link PMC2958627 Disease Relevance 0.19 Pain Relevance 0.20
In this regard, it has been shown that alternative inhibitors of GSK-3?
Negative_regulation (inhibitors) of GSK-3
11) Confidence 0.04 Published 2010 Journal Human Genomics and Proteomics : HGP Section Body Doc Link PMC2958627 Disease Relevance 0.47 Pain Relevance 0.28
-catenin through inhibition of GSK-3?
Negative_regulation (inhibition) of GSK-3
12) Confidence 0.04 Published 2010 Journal Human Genomics and Proteomics : HGP Section Body Doc Link PMC2958627 Disease Relevance 0.34 Pain Relevance 0.28
The inhibitory effect of lithium and VPA on GSK-3?
Negative_regulation (effect) of GSK-3
13) Confidence 0.04 Published 2010 Journal Human Genomics and Proteomics : HGP Section Body Doc Link PMC2958627 Disease Relevance 0.37 Pain Relevance 0.19
Therefore, the data indicate that ellagic acid stimulates apoptosis through inhibition of the pro-survival transcription factor NF-kB [46].
Negative_regulation (inhibition) of factor associated with apoptosis
14) Confidence 0.01 Published 2010 Journal International Journal of Environmental Research and Public Health Section Body Doc Link PMC2872306 Disease Relevance 1.43 Pain Relevance 0
Since no inhibition of nuclear factor (NF)-?
Negative_regulation (inhibition) of factor
15) Confidence 0.01 Published 2010 Journal International Journal of Environmental Research and Public Health Section Body Doc Link PMC2872306 Disease Relevance 0.80 Pain Relevance 0.16

General Comments

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