INT309150

From wiki-pain
Revision as of 17:32, 20 September 2012 by Daniel (Talk | contribs)

(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Jump to: navigation, search
Context Info
Confidence 0.03
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 8
Disease Relevance 3.46
Pain Relevance 3.09

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

nucleus (Edc4, Creb1) nucleoplasm (Creb1) mitochondrion (Creb1)
nucleolus (Creb1) DNA binding (Creb1) transcription factor binding (Creb1)
Anatomy Link Frequency
hippocampus 3
Edc4 (Rattus norvegicus)
Creb1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
bDMF 192 100.00 Very High Very High Very High
ischemia 536 99.56 Very High Very High Very High
Hippocampus 112 99.32 Very High Very High Very High
antagonist 64 95.12 Very High Very High Very High
anesthesia 32 5.00 Very Low Very Low Very Low
agonist 16 5.00 Very Low Very Low Very Low
cerebral cortex 8 5.00 Very Low Very Low Very Low
Pyramidal cell 8 5.00 Very Low Very Low Very Low
halothane 8 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Cv General 4 Under Development 472 99.56 Very High Very High Very High
Death 48 91.96 High High
Cognitive Disorder 128 89.72 High High
Apoptosis 40 60.44 Quite High
Targeted Disruption 72 55.44 Quite High
Cv Unclassified Under Development 48 5.00 Very Low Very Low Very Low
Stroke 48 5.00 Very Low Very Low Very Low
Middle Cerebral Artery Infarction 24 5.00 Very Low Very Low Very Low
Brain Hemorrhage 16 5.00 Very Low Very Low Very Low
Disease 16 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We also found that a second transcriptional target of CREB, Bcl-2, a potent antiapoptotic factor, was also induced by EDC in the hippocampal CA1 region following ischemic reperfusion (unpublished observation).
EDC Positive_regulation (induced) of CREB
1) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866326 Disease Relevance 0.12 Pain Relevance 0.13
The activation of CREB in the CA1 region by EDC following reperfusion was also observed at multiple time points (10min, 3h, 6h and 24h).
EDC Positive_regulation (activation) of CREB
2) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866326 Disease Relevance 0.70 Pain Relevance 0.40
Activation of CREB and enhanced levels of BDNF by EDC following GCI
EDC Positive_regulation (Activation) of CREB associated with ischemia and bdmf
3) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866326 Disease Relevance 0.54 Pain Relevance 0.44
As shown in Fig 7B&C, administration of the PI3K or MEK inhibitor markedly attenuated EDC-induced pCREB elevation in the CA1 region at 10min and 6h after reperfusion, as well as significantly attenuated the EDC-induced BDNF elevation at 6h after reperfusion, suggesting that PI3K-Akt and MEK-ERK signaling pathways mediate the EDC-induced elevation of pCREB and BDNF in the hippocampus following GCI.


EDC Positive_regulation (elevation) of pCREB in hippocampus associated with ischemia, hippocampus and bdmf
4) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866326 Disease Relevance 0.39 Pain Relevance 0.52
As shown in Fig. 7A, EDC rapidly increased pCREB levels in the CA1 region 10min post reperfusion, with a subsequent increase at 3h, 6h and 1d as compared to sham and vehicle controls.
EDC Positive_regulation (increased) of pCREB
5) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866326 Disease Relevance 0.45 Pain Relevance 0.43
As shown in Fig 7B&C, administration of the PI3K or MEK inhibitor markedly attenuated EDC-induced pCREB elevation in the CA1 region at 10min and 6h after reperfusion, as well as significantly attenuated the EDC-induced BDNF elevation at 6h after reperfusion, suggesting that PI3K-Akt and MEK-ERK signaling pathways mediate the EDC-induced elevation of pCREB and BDNF in the hippocampus following GCI.


EDC Positive_regulation (elevation) of pCREB in hippocampus associated with ischemia, hippocampus and bdmf
6) Confidence 0.02 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866326 Disease Relevance 0.36 Pain Relevance 0.47
The early elevation of pCREB levels by EDC, was followed by elevation of its transcriptional target, BDNF at latter time points (6h and 1d reperfusion) in the hippocampal CA1 region.
EDC Positive_regulation (elevation) of pCREB associated with bdmf
7) Confidence 0.02 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866326 Disease Relevance 0.35 Pain Relevance 0.42
The results of our study reveal that EDC and E2-BSA administered intracerebroventrically (icv) rapidly activates ERK, Akt and CREB signaling pathways in the hippocampus, enhances levels of the CREB transcriptional target, brain-derived neurotrophic factor (BDNF), strongly protects the hippocampal CA1 region against neuronal cell death, and significantly improves hippocampal-dependent cognitive function in the Morris water maze following GCI.
EDC Positive_regulation (activates) of CREB in hippocampus associated with cognitive disorder, ischemia, hippocampus, bdmf and death
8) Confidence 0.01 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866326 Disease Relevance 0.54 Pain Relevance 0.28

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox