INT54588

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Context Info
Confidence 0.67
First Reported 1994
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 38
Total Number 42
Disease Relevance 12.01
Pain Relevance 9.18

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

nucleoplasm (CREB1) signal transduction (CREB1) mitochondrion (CREB1)
nucleolus (CREB1) nucleus (CREB1) transcription factor binding (CREB1)
Anatomy Link Frequency
neuronal 6
chondrocytes 2
brain 1
bladder 1
DRG 1
CREB1 (Homo sapiens)
Pain Link Frequency Relevance Heat
alcohol 306 100.00 Very High Very High Very High
nMDA receptor 24 100.00 Very High Very High Very High
spinal dorsal horn 3 99.68 Very High Very High Very High
GABAergic 12 99.32 Very High Very High Very High
tolerance 3 98.80 Very High Very High Very High
Osteoarthritis 160 98.34 Very High Very High Very High
cytokine 176 98.32 Very High Very High Very High
Kinase C 3 98.30 Very High Very High Very High
addiction 10 98.24 Very High Very High Very High
GABA receptor 30 98.08 Very High Very High Very High
Disease Link Frequency Relevance Heat
Hypersensitivity 29 99.90 Very High Very High Very High
Cystitis 29 99.00 Very High Very High Very High
Stress 154 98.84 Very High Very High Very High
Osteoarthritis 160 98.34 Very High Very High Very High
Nervous System Injury 5 98.24 Very High Very High Very High
Alcoholic Liver Diseases 19 98.16 Very High Very High Very High
Hepatitis B Virus Infection 2 98.08 Very High Very High Very High
Hepatitis C Virus Infection 27 97.60 Very High Very High Very High
Injury 68 97.12 Very High Very High Very High
Neuropathic Pain 22 94.08 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In this category are drugs that increase cyclic AMP-responsive element binding protein (CREB), the activity of which is known to contribute to important neuronal functions, such as synaptic plasticity, learning and memory (Farah et al., 2004).
Positive_regulation (increase) of CREB in neuronal
1) Confidence 0.67 Published 2007 Journal Med Health Care Philos Section Body Doc Link PMC2779437 Disease Relevance 0.12 Pain Relevance 0
In this category are drugs that increase cyclic AMP-responsive element binding protein (CREB), the activity of which is known to contribute to important neuronal functions, such as synaptic plasticity, learning and memory (Farah et al., 2004).
Positive_regulation (increase) of cyclic AMP-responsive element binding protein in neuronal
2) Confidence 0.67 Published 2007 Journal Med Health Care Philos Section Body Doc Link PMC2779437 Disease Relevance 0.12 Pain Relevance 0
NORF was less effective but did significantly increase phospho-CREB at a concentration of 200 nM.
Positive_regulation (increase) of CREB
3) Confidence 0.50 Published 2007 Journal Biochem. Pharmacol. Section Abstract Doc Link 17382299 Disease Relevance 0 Pain Relevance 0.45
Our data demonstrate a close association between the expression of behavioral hypersensitivity and cyclic AMP response element-binding protein activation in the spinal dorsal horn following spared nerve injury, supporting the notion that phosphorylated cyclic AMP response element-binding protein may play an important role in the maintenance of chronic neuropathic pain.
Positive_regulation (activation) of cyclic AMP response element-binding protein in dorsal horn associated with nervous system injury, spinal dorsal horn, hypersensitivity and neuropathic pain
4) Confidence 0.50 Published 2006 Journal Neuroscience Section Abstract Doc Link 16515839 Disease Relevance 0.63 Pain Relevance 0.43
Annexin V, RGS4 and CREB genes showed pronounced increase in expression after stimulation with DAMGO.
Positive_regulation (increase) of CREB
5) Confidence 0.45 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16377088 Disease Relevance 0.09 Pain Relevance 0.77
Induction of a dominant negative CREB transgene specifically blocks long-term memory in Drosophila.
Positive_regulation (Induction) of CREB
6) Confidence 0.45 Published 1994 Journal Cell Section Title Doc Link 7923376 Disease Relevance 0 Pain Relevance 0.09
Following the end of ethanol exposure (P30), neocortical development and plasticity may be further disrupted as a result of substantial and long-lasting alterations of CREB activity [70]–[73], NMDA receptor activation [10], [26], and GABAergic mediated inhibition [24], [25], [74], [75].
Positive_regulation (activation) of CREB associated with gabaergic and nmda receptor
7) Confidence 0.35 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2721629 Disease Relevance 0 Pain Relevance 0.46
Our recent findings [35] and other studies [36], [37] suggest that phosphodiesterase (PDE) inhibitors might be good candidates for enhancing CREB activation.
Positive_regulation (activation) of CREB
8) Confidence 0.35 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2721629 Disease Relevance 0 Pain Relevance 0.17
Therefore, intervening directly with CREB activation during development may ultimately allow for the maturation of sensory maps.
Positive_regulation (activation) of CREB
9) Confidence 0.35 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2721629 Disease Relevance 0 Pain Relevance 0.19
In other words, NMDA and GABA receptors must be functional at some level, since systemic administration of vinpocetine resulted in the restoration of pCREB to cortical cells indiscriminately, yielding the recovery of cortical orientation selectivity.
Positive_regulation (restoration) of pCREB associated with gaba receptor
10) Confidence 0.33 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2721629 Disease Relevance 0 Pain Relevance 0.34
In conclusion, we showed that administration of a PDE1 inhibitor several days after the period of alcohol exposure can improve cortical organization in the ferret model of FASD by restoring pCREB levels.
Positive_regulation (restoring) of pCREB associated with alcohol
11) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2721629 Disease Relevance 0 Pain Relevance 0.17
When pCREB levels of alcohol exposed animals were restored during vinpocetine treatment, concomitantly visual activity triggered cortical cells and this activation was able to be translated into plastic changes that resulted in the normal refinement of cortical maps.
Positive_regulation (restored) of pCREB associated with alcohol
12) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2721629 Disease Relevance 0 Pain Relevance 0.45
In the absence of PKA inhibitors, isoproterenol increased the phosphorylation state of CREB within 5 min returning to basal after 60 min (n = 3).
Positive_regulation (state) of CREB
13) Confidence 0.28 Published 2005 Journal Cell Commun Signal Section Body Doc Link PMC1198236 Disease Relevance 0.12 Pain Relevance 0.06
CREB is a well characterized transcriptional factor, which is activated by cAMP-dependent PKA phosphorylation of specific serine residues [16].
Positive_regulation (activated) of CREB
14) Confidence 0.28 Published 2005 Journal Cell Commun Signal Section Body Doc Link PMC1198236 Disease Relevance 0.07 Pain Relevance 0.04
IGF-I regulates survival at the nuclear level through accumulation of phospho-Akt in DRG neuronal nuclei, increased CREB-mediated transcription, and nuclear exclusion of FKHR.
Positive_regulation (increased) of CREB in neuronal
15) Confidence 0.26 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2663454 Disease Relevance 1.08 Pain Relevance 0.06
For neuronal cells, it has been suggested that a subpopulation of classical RAR receptors, localized at or near the cell membrane, could be responsible for ATRA-induced CREB (cyclic AMP-response-element-binding protein) activation through ERK1/2 phosphorylation [14].
Positive_regulation (activation) of CREB in neuronal
16) Confidence 0.24 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC1769480 Disease Relevance 0.20 Pain Relevance 0.03
For neuronal cells, it has been suggested that a subpopulation of classical RAR receptors, localized at or near the cell membrane, could be responsible for ATRA-induced CREB (cyclic AMP-response-element-binding protein) activation through ERK1/2 phosphorylation [14].
Positive_regulation (activation) of cyclic AMP-response-element-binding protein in neuronal
17) Confidence 0.24 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC1769480 Disease Relevance 0.20 Pain Relevance 0.03
Furthermore, we found that the CaM kinase IV cascade is also involved in the regulation of CREB activation by the mood stabilizer lithium [32].
Positive_regulation (activation) of CREB
18) Confidence 0.18 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2483719 Disease Relevance 0.11 Pain Relevance 0.17
Gene-dosage experiments in transiently transfected HEK293 cells demonstrated that both human isoforms of GPR17 inhibited a forskolin-induced CREB activity with approximately 75% (Figure 3A,B).
Positive_regulation (induced) of CREB
19) Confidence 0.17 Published 2010 Journal British Journal of Pharmacology Section Body Doc Link PMC2839267 Disease Relevance 0.08 Pain Relevance 0.05
q also mediate CREB activation (Shaywitz and Greenberg, 1999).
Positive_regulation (mediate) of CREB
20) Confidence 0.17 Published 2010 Journal British Journal of Pharmacology Section Body Doc Link PMC2839267 Disease Relevance 0.06 Pain Relevance 0.09

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