INT228670

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.38
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 12
Total Number 14
Disease Relevance 5.27
Pain Relevance 1.21

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
neuronal 1
hypothalamus 1
brain 1
Rps6kb1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
wide dynamic range 33 96.32 Very High Very High Very High
c fibre 60 95.08 Very High Very High Very High
Spinal cord 84 86.44 High High
Inflammatory response 1 81.92 Quite High
Glutamate 3 78.16 Quite High
Sciatic nerve 5 75.84 Quite High
withdrawal 35 71.64 Quite High
cytokine 14 70.60 Quite High
Inflammation 21 70.20 Quite High
Gabapentin 3 68.40 Quite High
Disease Link Frequency Relevance Heat
Injury 121 99.76 Very High Very High Very High
Cardiovascular Disease 12 99.28 Very High Very High Very High
Hyperplasia 24 99.18 Very High Very High Very High
Neointima 66 95.96 Very High Very High Very High
Neuropathic Pain 54 92.62 High High
Nervous System Injury 47 92.40 High High
Diabetes Mellitus 44 87.88 High High
Obesity 84 85.72 High High
Hypersensitivity 76 84.08 Quite High
Insulin Resistance 12 84.04 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Rapamycin eluting stents have proven to significantly reduce the rate of coronary stent restenosis in human clinical trials.8 Through inactivation of p70S6 kinase (P70S6K) and eukaryocytic initiation factor 4E (eIF4E), rapamycin increases the activity of p27Kip1 and RB.9,10 The mTOR itself is known to be activated by the phosphoinositide 3-kinase (PI3K)-Akt pathway.11,12
Negative_regulation (inactivation) of P70S6K associated with cardiovascular disease
1) Confidence 0.38 Published 2008 Journal Yonsei Medical Journal Section Body Doc Link PMC2615285 Disease Relevance 0.52 Pain Relevance 0.10
Rapamycin eluting stents have proven to significantly reduce the rate of coronary stent restenosis in human clinical trials.8 Through inactivation of p70S6 kinase (P70S6K) and eukaryocytic initiation factor 4E (eIF4E), rapamycin increases the activity of p27Kip1 and RB.9,10 The mTOR itself is known to be activated by the phosphoinositide 3-kinase (PI3K)-Akt pathway.11,12
Negative_regulation (inactivation) of p70S6 kinase associated with cardiovascular disease
2) Confidence 0.38 Published 2008 Journal Yonsei Medical Journal Section Body Doc Link PMC2615285 Disease Relevance 0.52 Pain Relevance 0.10
By inactivating P70S6K and eIF4E, rapamycin increases the activity of p27Kip1 and RB, subsequently resulting in inhibition of VSMC proliferation.
Negative_regulation (inactivating) of P70S6K
3) Confidence 0.38 Published 2008 Journal Yonsei Medical Journal Section Body Doc Link PMC2615285 Disease Relevance 0.54 Pain Relevance 0.06
Effects of PI3K or MEK inhibitors on Akt-mTOR-P70S6K in RAoSMCs treated with rosiglitazone
Negative_regulation (inhibitors) of mTOR-P70S6K
4) Confidence 0.38 Published 2008 Journal Yonsei Medical Journal Section Body Doc Link PMC2615285 Disease Relevance 1.09 Pain Relevance 0.04
Compared to cells treated with insulin alone, cells treated with rosiglitazone before insulin stimulus demonstrated a significant inhibitory effect on the proteins upstream, Akt, and downstream, P70S6K, of mTOR.
Negative_regulation (effect) of P70S6K
5) Confidence 0.37 Published 2008 Journal Yonsei Medical Journal Section Body Doc Link PMC2615285 Disease Relevance 0.92 Pain Relevance 0.03
In conclusion, rosiglitazone inhibits neointimal hyperplasia after carotid balloon injury because it blocks the Akt-mTOR-P70S6 kinase pathway, resulting in inhibition of VSMC proliferation.
Negative_regulation (blocks) of P70S6 kinase associated with injury and hyperplasia
6) Confidence 0.37 Published 2008 Journal Yonsei Medical Journal Section Body Doc Link PMC2615285 Disease Relevance 0.89 Pain Relevance 0.03
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.
Negative_regulation (reduction) of p70S6K in neuronal associated with neuropathic pain
7) Confidence 0.33 Published 2010 Journal The Journal of Pain Section Body Doc Link PMC3000494 Disease Relevance 0.16 Pain Relevance 0.19
Although not investigated further in this study, we are also confident that the results produced in our electrophysiological and behavioral data reflect a reduction in p70S6K activity.
Negative_regulation (reduction) of p70S6K
8) Confidence 0.33 Published 2010 Journal The Journal of Pain Section Body Doc Link PMC3000494 Disease Relevance 0.36 Pain Relevance 0.12
Exercised animals pretreated with Rapamycin also reduced hypothalamic p70S6K and 4EBP1 phosphorylation (Figures 8d and e).
Negative_regulation (reduced) of p70S6K
9) Confidence 0.29 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2585815 Disease Relevance 0 Pain Relevance 0
AICAR reduced p70S6K and 4EBP1 threonine phosphorylation levels in the hypothalamus of control and exercised rats.
Negative_regulation (reduced) of p70S6K in hypothalamus
10) Confidence 0.29 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2585815 Disease Relevance 0 Pain Relevance 0.03
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.
Negative_regulation (decrease) of p70S6K in brain associated with neuropathic pain
11) Confidence 0.29 Published 2010 Journal The Journal of Pain Section Body Doc Link PMC3000494 Disease Relevance 0.18 Pain Relevance 0.26
The level of phosphorylation of S6 protein was also used as a measure of S6K activity [23], [32]–[34].
Negative_regulation (measure) of S6K
12) Confidence 0.22 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2276314 Disease Relevance 0.08 Pain Relevance 0.25
Protein and phosphorylation levels of AKT, p70 S6K and 4E-BP1
Negative_regulation (levels) of p70 S6K
13) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2736646 Disease Relevance 0 Pain Relevance 0
0.097), and moreover, elements examined downstream of AKT (phosphorylation levels of p70 S6K and 4E-BP1) were unchanged by the LPS treatment protocol described here.
Negative_regulation (levels) of p70 S6K
14) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2736646 Disease Relevance 0 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox