INT174069

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Context Info
Confidence 0.61
First Reported 2003
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 14
Total Number 15
Disease Relevance 3.70
Pain Relevance 0.77

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

signal transduction (Rps6kb1) mitochondrion (Rps6kb1) aging (Rps6kb1)
nucleus (Rps6kb1) cell cycle (Rps6kb1) cytoplasm (Rps6kb1)
Anatomy Link Frequency
dorsal 2
neuronal 1
myocardium 1
neurons 1
Rps6kb1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
agonist 25 91.36 High High
Hippocampus 101 91.32 High High
wide dynamic range 22 84.80 Quite High
c fibre 40 83.56 Quite High
Inflammation 18 79.04 Quite High
withdrawal 16 76.64 Quite High
Spinal cord 56 74.92 Quite High
Glutamate 2 66.64 Quite High
long-term potentiation 42 62.40 Quite High
gABA 2 52.32 Quite High
Disease Link Frequency Relevance Heat
Neuropathic Pain 34 99.30 Very High Very High Very High
Neointima 66 99.20 Very High Very High Very High
Cancer 6 97.88 Very High Very High Very High
Hyperplasia 24 95.84 Very High Very High Very High
Anxiety Disorder 9 95.68 Very High Very High Very High
Heart Rate Under Development 10 95.16 Very High Very High Very High
Diabetes Mellitus 43 94.88 High High
Hyperglycemia 12 92.40 High High
Injury 106 91.96 High High
Insulin Resistance 12 90.00 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Fig. 3 shows that the activation of the Akt-mTOR-P70S6K pathway was significantly increased after treatment with 1 ┬ÁM of insulin for 15 mins.
Positive_regulation (activation) of mTOR-P70S6K
1) Confidence 0.61 Published 2008 Journal Yonsei Medical Journal Section Body Doc Link PMC2615285 Disease Relevance 0.58 Pain Relevance 0
Second, they demonstrate that one of the main effects of BDNF action during memory formation is to increase the expression of GluR1 in synaptic membranes, and that it does so by activating the translation machinery through the engagement of mTOR and its downstream target p70S6K.
Positive_regulation (activating) of p70S6K
2) Confidence 0.42 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2695538 Disease Relevance 0.05 Pain Relevance 0.11
This suggests that rosiglitazone significantly inhibits the activation of the Akt-mTOR-P70S6K system.


Positive_regulation (activation) of mTOR-P70S6K
3) Confidence 0.41 Published 2008 Journal Yonsei Medical Journal Section Body Doc Link PMC2615285 Disease Relevance 1.03 Pain Relevance 0.04
The results in the present study demonstrated that cells treated with rosiglitazone before insulin stimulus exhibited significant inhibition of p-mTOR, p-Akt, and p-P70S6K, indicating significant inhibition of the activation of the Akt-mTOR-P70S6K system.
Positive_regulation (activation) of mTOR-P70S6K
4) Confidence 0.41 Published 2008 Journal Yonsei Medical Journal Section Body Doc Link PMC2615285 Disease Relevance 0.12 Pain Relevance 0.05
significant inhibition of activation of p-Akt, p-m-TOR, and p-p70S6K in cells treated with rosiglitazone.
Positive_regulation (activation) of p70S6K
5) Confidence 0.41 Published 2008 Journal Yonsei Medical Journal Section Abstract Doc Link PMC2615285 Disease Relevance 0.32 Pain Relevance 0
Inhibition of both MEK and PI3K resulted in partial reduction of p-P70S6K expression that was associated with additional inhibition, indicating that both the MAPK and PI3K pathways have an effect on the activation of the Akt-mTOR-P70S6K system.


Positive_regulation (activation) of mTOR-P70S6K
6) Confidence 0.41 Published 2008 Journal Yonsei Medical Journal Section Body Doc Link PMC2615285 Disease Relevance 0.52 Pain Relevance 0.04
The relatively restricted neuronal localization of activated phospho p70S6K is also of interest because these neurons double label for PKC?
Positive_regulation (activated) of p70S6K in neurons
7) Confidence 0.39 Published 2010 Journal The Journal of Pain Section Body Doc Link PMC3000494 Disease Relevance 0.45 Pain Relevance 0.09
In addition, we found that pre- or post-training administration of function-blocking anti-BDNF antibodies into dorsal CA1 hampered IA LTM retention, abolished the learning-induced biphasic activation of mTOR and its readout, p70S6K and blocked GluR1 expression, indicating that BDNF is an upstream factor controlling mTOR signaling during fear-memory consolidation.
Positive_regulation (activation) of p70S6K in dorsal associated with anxiety disorder
8) Confidence 0.39 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2695538 Disease Relevance 0.10 Pain Relevance 0.04
To investigate the effect of learning on the activation of mTOR and its downstream effector p70S6K we used a one-trial step-down inhibitory avoidance paradigm (IA).
Positive_regulation (activation) of p70S6K
9) Confidence 0.39 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2695538 Disease Relevance 0.09 Pain Relevance 0.07
We found that blockade of BDNF with function-blocking anti-BDNF antibodies delivered into dorsal CA1 15 min before training abolished the IA learning-induced increase in mTOR (Figure 5A) and p70S6K (Figure 5B) phosphorylation.
Positive_regulation (increase) of p70S6K in dorsal
10) Confidence 0.39 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2695538 Disease Relevance 0 Pain Relevance 0.06
Our finding that SNL results in a decrease in immunoreactivity for phospho p70S6K in the corresponding lumbar spinal segment (L5) is of particular interest because intuitively, based on previous studies, particularly concerning neuronal activity in the brain, a condition like neuropathy would be expected to result in an increase in phospho p70S6K immunoreactivity.5,21,35,36 Intriguingly, one-third of lamina II interneurons receive simultaneous monosynaptic inputs from 2 to 4 different segmental roots.23 This model of organization, where substantia gelatinosia spinal neurons at L4 receive major monosynaptic input from L4-L6 roots, suggests that the reduction in L5 phospho p70S6K and CGRP immunoreactivity after SNL should also be observed in L4 (even though at this level, spinal nerves are not ligated) and that neurons within L4 will have reduced responses.
Positive_regulation (increase) of p70S6K in neuronal associated with neuropathic pain
11) Confidence 0.34 Published 2010 Journal The Journal of Pain Section Body Doc Link PMC3000494 Disease Relevance 0.18 Pain Relevance 0.23
However, if real, reduced AKT Ser473 phosphorylation would appear to have had no significant impact on the two downstream translation initiation intermediates p70 S6K and 4E-BP1.
Neg (no) Positive_regulation (intermediates) of p70 S6K
12) Confidence 0.25 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2736646 Disease Relevance 0 Pain Relevance 0
Firstly, elevated phosphorylation levels of residues Thr421 and Ser424 for p70 S6K were observed in the myocardium of LPS-treated rats. p70 S6K indirectly promotes the translation of target oligopyrimidine (TOP) mRNAs which are almost exclusively confined to transcripts that encode for ribosomal proteins and translation factors.
Positive_regulation (elevated) of p70 S6K in myocardium
13) Confidence 0.25 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2736646 Disease Relevance 0.17 Pain Relevance 0
Namely, it has been known that insulin receptor signaling results in activation of PI3K and a variety of downstream effectors, including Akt, mTOR, and P70S6K, after insulin binds to insulin receptors located on the cell membrane.
Positive_regulation (activation) of P70S6K
14) Confidence 0.18 Published 2008 Journal Yonsei Medical Journal Section Body Doc Link PMC2615285 Disease Relevance 0.11 Pain Relevance 0.04
Insulin and IGF-1 receptors activate several different regulatory proteins, including RAS, MAP kinase, PI3 kinase, S6 kinase and protein tyrosine phosphatase [6,7,17].
Positive_regulation (activate) of S6 kinase
15) Confidence 0.02 Published 2003 Journal BMC Neurosci Section Body Doc Link PMC165579 Disease Relevance 0 Pain Relevance 0

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