INT211591

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Context Info
Confidence 0.57
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 14
Total Number 17
Disease Relevance 5.73
Pain Relevance 3.26

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

mitochondrion (PSEN1) Golgi apparatus (PSEN1) endoplasmic reticulum (PSEN1)
embryo development (PSEN1) peptidase activity (PSEN1) cell death (PSEN1)
Anatomy Link Frequency
cleavage 2
fibroblasts 2
PSEN1 (Homo sapiens)
PSEN1 - M146L (2) PSEN1 - G384A (1)
Pain Link Frequency Relevance Heat
bradykinin 150 100.00 Very High Very High Very High
Pain 215 99.98 Very High Very High Very High
cINOD 60 94.92 High High
Pain score 30 89.28 High High
Dismenorea 114 87.56 High High
Analgesic 24 85.76 High High
Lasting pain 3 70.40 Quite High
Eae 16 65.08 Quite High
aspirin 21 24.80 Low Low
addiction 4 11.20 Low Low
Disease Link Frequency Relevance Heat
Pain 257 99.98 Very High Very High Very High
Disease 493 99.64 Very High Very High Very High
Stress 204 95.12 Very High Very High Very High
INFLAMMATION 47 94.68 High High
Alzheimer's Dementia 58 88.60 High High
Dysmenorrhea 114 87.56 High High
Targeted Disruption 25 85.36 High High
Gastrointestinal Disease 6 70.64 Quite High
Respiratory Disease 6 68.96 Quite High
Reprotox - General 1 18 67.32 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The evidence that mutations in PSEN1/PSEN2 that cause Familial Alzheimer's disease are loss of function mutants, and that loss of PSEN1/PSEN2 function causes neurodegeneration in mice, supports this hypothesis [49], [50], [51], [52], [53].
Negative_regulation (loss) of PSEN1 associated with disease
1) Confidence 0.57 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2905372 Disease Relevance 0.87 Pain Relevance 0.03
Specifically, the Notch cleavage activities of PS1-D385TG, PS1-DTG/DTG, PS1-D257TG and PS1-M146V have decreased by about 62%, 46%, 22% and 7%, respectively, compared to PS1wt activity (Figure 5).
Negative_regulation (decreased) of PS1-M146V (M146V) in cleavage
2) Confidence 0.35 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2405781 Disease Relevance 0 Pain Relevance 0
Development of APP/PS1 Stable Cell Lines
Negative_regulation (Development) of PS1
3) Confidence 0.35 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2405781 Disease Relevance 0 Pain Relevance 0
42 production was only partially reduced in PS1-D385TG-expressing cells under the same treatment conditions (Figure 4, lane 4).
Negative_regulation (reduced) of PS1-D385TG
4) Confidence 0.35 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2405781 Disease Relevance 0 Pain Relevance 0.07
In fact, complete deficiency of PS1 in mice abolishes the processing of both APP to release A?
Negative_regulation (deficiency) of PS1
5) Confidence 0.35 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2405781 Disease Relevance 0.32 Pain Relevance 0
Interestingly, the clinical PS1 G384A mutant increased A?
Negative_regulation (clinical) of PS1 (G384A)
6) Confidence 0.35 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2405781 Disease Relevance 0 Pain Relevance 0
42 in PS1-D385TG is not due to the conversion of PS1 into a classic aspartyl protease because the mutated triplet D385TA still increases production of A?
Negative_regulation (conversion) of PS1
7) Confidence 0.35 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2405781 Disease Relevance 0 Pain Relevance 0
Activation of ERK was substantially diminished at both 25 nM and 250 nM BK in PS-1 (M146L) AD fibroblasts (Figure 3A–C).
Negative_regulation (diminished) of PS-1 (M146L) in fibroblasts associated with disease and bradykinin
8) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2644820 Disease Relevance 0.72 Pain Relevance 0.25
Yet the magnitude of p38 activation was still significantly decreased in PS-1 (M146L) AD fibroblasts compared to normal controls.
Negative_regulation (decreased) of PS-1 (M146L) in fibroblasts associated with disease
9) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2644820 Disease Relevance 0.92 Pain Relevance 0.32
Starting from the treatment cycle 3, both the overall-pain and the peak-pain intensity reduced in the FAD group and rose in the placebo group.
Negative_regulation (reduced) of FAD associated with pain
10) Confidence 0.16 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1940310 Disease Relevance 0.68 Pain Relevance 0.76
At treatment cycle 3, the pain intensity was decreased in the FAD group and increased in the placebo group; the changes persisted to the treatment cycle 4 and follow-up cycle 1.
Negative_regulation (decreased) of FAD associated with pain
11) Confidence 0.16 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1940310 Disease Relevance 1.22 Pain Relevance 1.22
The GEE model (Figure 2) fitted with the explanatory variables, treatment and cycle, by the approach with “unstructured working correlation” [21], shows trends of peak-pain decreasing in the FAD group and increasing in the placebo group.
Negative_regulation (decreasing) of FAD associated with pain
12) Confidence 0.16 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1940310 Disease Relevance 0.64 Pain Relevance 0.43
Inhibition of MCMJR1 by an established presenilin transition state analog inhibitor
Negative_regulation (inhibitor) of presenilin
13) Confidence 0.16 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947513 Disease Relevance 0.07 Pain Relevance 0.07
Specifically, the Notch cleavage activities of PS1-D385TG, PS1-DTG/DTG, PS1-D257TG and PS1-M146V have decreased by about 62%, 46%, 22% and 7%, respectively, compared to PS1wt activity (Figure 5).
Negative_regulation (decreased) of PS1-D257TG in cleavage
14) Confidence 0.15 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2405781 Disease Relevance 0 Pain Relevance 0
Here we asked the question of whether established inhibitors of presenilin and SPP could also have an effect on MCMJR1.
Negative_regulation (inhibitors) of presenilin
15) Confidence 0.13 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947513 Disease Relevance 0.09 Pain Relevance 0.09
In presenilin, the corresponding mutant (G384A) significantly decreases the rate of production of A?
Negative_regulation (decreases) of presenilin
16) Confidence 0.12 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947513 Disease Relevance 0 Pain Relevance 0
Finally, an established presenilin and SPP transition-state analog inhibitor could inhibit MCMJR1.


Negative_regulation (inhibitor) of presenilin
17) Confidence 0.06 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2947513 Disease Relevance 0.20 Pain Relevance 0

General Comments

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