INT136692

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Context Info
Confidence 0.78
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 12
Total Number 13
Disease Relevance 2.14
Pain Relevance 3.65

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

nucleoplasm (Akt1) transport (Akt1) aging (Akt1)
enzyme binding (Akt1) carbohydrate metabolic process (Akt1) cytoplasm (Akt1)
Anatomy Link Frequency
myocardium 1
hepatocytes 1
spinal cord 1
IB4 1
Akt1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Bile 61 99.84 Very High Very High Very High
qutenza 6 99.64 Very High Very High Very High
Paracetamol 180 99.46 Very High Very High Very High
Opioid 2 98.24 Very High Very High Very High
withdrawal 2 97.96 Very High Very High Very High
Calcitonin gene-related peptide 1 97.76 Very High Very High Very High
Spinal cord 32 97.24 Very High Very High Very High
imagery 22 89.32 High High
Pain 5 88.32 High High
ischemia 16 82.40 Quite High
Disease Link Frequency Relevance Heat
Opiate Addiction 1 98.24 Very High Very High Very High
Nociception 2 94.52 High High
Pain 3 88.32 High High
Aging 114 82.16 Quite High
Injury 28 81.20 Quite High
Cv General 4 Under Development 4 79.68 Quite High
Hyperalgesia 1 79.68 Quite High
INFLAMMATION 1 79.16 Quite High
Fistula 19 78.80 Quite High
Cv Unclassified Under Development 9 76.20 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
It clearly documents a significant role of ROS signaling in Akt/eNOS/Cav-3-mediated GLUT-4 translocation and association in IP myocardium.
Localization (translocation) of Akt in myocardium
1) Confidence 0.78 Published 2007 Journal Am. J. Physiol. Heart Circ. Physiol. Section Abstract Doc Link 17277024 Disease Relevance 0.15 Pain Relevance 0.19
After capsaicin injection, p-PKB/Akt (473) is colocalized with isotectin-B4 (IB4), tyrosine kinase A (TrkA), and calcitonin gene-related peptide (CGRP).
Localization (colocalized) of Akt in IB4 associated with qutenza and calcitonin gene-related peptide
2) Confidence 0.73 Published 2007 Journal Neuroscience Section Abstract Doc Link 17084039 Disease Relevance 0.40 Pain Relevance 0.85
Unlike that observed for iNOS, acetaminophen did not appear to affect the regulation of nNOS or eNOS expression (Figure 5B) suggesting perhaps that the normalization of Akt S-nitrosylation by acetaminophen may be dependent on the reduced expression of iNOS.
Localization (normalization) of Akt associated with paracetamol
3) Confidence 0.72 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2712760 Disease Relevance 0.19 Pain Relevance 0.50
As such, it is likely that the S-nitrosylation of Akt is involved in contributing to age-associated Akt dysfunction.
Localization (nitrosylation) of Akt
4) Confidence 0.72 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2712760 Disease Relevance 0.25 Pain Relevance 0.48
After 6 months of acetaminophen treatment, S-nitrosylated Akt abundance was restored to that of 27-month animals (P>0.05).
Localization (abundance) of Akt associated with paracetamol
5) Confidence 0.63 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2712760 Disease Relevance 0.13 Pain Relevance 0.47
Moreover, the downstream signaling molecule of Akt, GSK3?
Localization (molecule) of Akt
6) Confidence 0.59 Published 2010 Journal BMC Neurol Section Body Doc Link PMC3020671 Disease Relevance 0 Pain Relevance 0
Increased prostaglandin E2 release and activated Akt/beta-catenin signaling pathway occur after opioid withdrawal in rat spinal cord.
Localization (release) of Akt in spinal cord associated with withdrawal, opioid and spinal cord
7) Confidence 0.54 Published 2006 Journal Anesthesiology Section Title Doc Link 16810007 Disease Relevance 0.19 Pain Relevance 0.38
Our immunofluorescence staining localizes increased pAkt and pGSK3?
Localization (localizes) of pAkt
8) Confidence 0.49 Published 2010 Journal BMC Neurol Section Body Doc Link PMC3020671 Disease Relevance 0.22 Pain Relevance 0.04
The activation of ERK1/2 and AKT signaling pathways by bile acids in hepatocytes appears not to involve the GPCR TGR5, because its gene is not highly expressed in hepatocytes, is G?
Localization (pathways) of AKT in hepatocytes associated with bile
9) Confidence 0.45 Published 2010 Journal Journal of Lipid Research Section Body Doc Link PMC2903791 Disease Relevance 0.08 Pain Relevance 0.31
Membranes were incubated with antibodies for Akt (Cell Signaling Technology, MA, USA), SytI (BD Biosciences), MafK/NF-E2 p18 (Santa Cruz Biotechnology, CA, USA), Syn-1 (Millipore, CA, USA), ?
Localization (incubated) of Akt
10) Confidence 0.41 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2844376 Disease Relevance 0.13 Pain Relevance 0.07
It has also been shown that Akt can be localized to mitochondria and can phosphorylate the ?
Localization (localized) of Akt
11) Confidence 0.39 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2467486 Disease Relevance 0 Pain Relevance 0.13
-mercaptoethanol) before re-blotting with rabbit anti-Akt (1?
Localization (blotting) of Akt
12) Confidence 0.35 Published 2010 Journal PLoS Biology Section Body Doc Link PMC2889931 Disease Relevance 0 Pain Relevance 0.08
FBS- and PDGF-BB-stimulated intracellular Ras, MEK1/2, ERK1/2, proliferative cell nuclear antigen (PCNA), and Akt activations were significantly inhibited by lercanidipine; however, lercanidipine did not affect FBS- and PDGF-BB-induced STAT3 phosphorylation.
Localization (activations) of Akt
13) Confidence 0.15 Published 2009 Journal Pharmacol. Res. Section Abstract Doc Link 18973813 Disease Relevance 0.41 Pain Relevance 0.14

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