INT11625

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Context Info
Confidence 0.78
First Reported 1992
Last Reported 2011
Negated 0
Speculated 1
Reported most in Body
Documents 98
Total Number 109
Disease Relevance 55.46
Pain Relevance 20.86

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

cell adhesion (App) Golgi apparatus (App) plasma membrane (App)
extracellular matrix organization (App) DNA binding (App) cytoplasm (App)
Anatomy Link Frequency
cleavage 7
neurons 7
synapse 5
plasma 2
dendrites 2
App (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 811 100.00 Very High Very High Very High
cytokine 332 100.00 Very High Very High Very High
Abeta 143 100.00 Very High Very High Very High
Inflammatory mediators 42 99.90 Very High Very High Very High
tetrodotoxin 25 99.48 Very High Very High Very High
Intracerebroventricular 2 99.32 Very High Very High Very High
opiate 4 99.22 Very High Very High Very High
cINOD 354 99.20 Very High Very High Very High
Kinase C 232 98.66 Very High Very High Very High
long-term potentiation 114 98.04 Very High Very High Very High
Disease Link Frequency Relevance Heat
Alzheimer's Dementia 1476 100.00 Very High Very High Very High
INFLAMMATION 1043 100.00 Very High Very High Very High
Watson Syndrome 56 100.00 Very High Very High Very High
Immunization 39 100.00 Very High Very High Very High
Targeted Disruption 1565 99.96 Very High Very High Very High
Adhesions 97 99.92 Very High Very High Very High
Disease 4273 99.76 Very High Very High Very High
Sprains And Strains 86 98.88 Very High Very High Very High
Hypersensitivity 132 98.16 Very High Very High Very High
Toxicity 182 97.68 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The degree of decrease was more pronounced in APP/PS1 mice at frequencies greater than 1 Hz (Fig. 4A), indicating existence of compromised SR storage and release of intracellular Ca2+ in APP/PS1 mouse hearts.


Localization (release) of APP/PS1 in hearts
1) Confidence 0.78 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2696039 Disease Relevance 0.19 Pain Relevance 0
The mutations that have been found to be responsible for these cases of familial Alzheimer disease (FAD) are localized on the APP, PS1 or PS2 genes.
Localization (localized) of APP associated with alzheimer's dementia
2) Confidence 0.75 Published 2007 Journal Acta Neuropathol Section Body Doc Link PMC2100431 Disease Relevance 0.84 Pain Relevance 0
The available evidence has shown that intracellular trafficking of APP is regulated by a number of factors.
Localization (trafficking) of APP
3) Confidence 0.75 Published 2011 Journal Mol Brain Section Body Doc Link PMC3022812 Disease Relevance 0.14 Pain Relevance 0.07
Co-expression of ADAM9 with APP promoted sAPP?
Localization (sAPP) of APP
4) Confidence 0.75 Published 2011 Journal Mol Brain Section Body Doc Link PMC3022812 Disease Relevance 0.14 Pain Relevance 0.06
APP was found to colocalize with ?
Localization (colocalize) of APP
5) Confidence 0.75 Published 2011 Journal Mol Brain Section Body Doc Link PMC3022812 Disease Relevance 0.23 Pain Relevance 0
The cleavage of APP by presenilins, which generates A?
Localization (cleavage) of APP in cleavage
6) Confidence 0.75 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2912762 Disease Relevance 1.33 Pain Relevance 0.03
Radiolabeling SNs with 35S-Met and immunoprecipitation of APP.
Localization (immunoprecipitation) of APP
7) Confidence 0.74 Published 2007 Journal PLoS Biology Section Body Doc Link PMC1808499 Disease Relevance 0.20 Pain Relevance 0.08
In conclusion, FMRP represses translation of APP mRNA in dendrites, suggesting a link between two neurodevelopmental disorders, FXS and autism, and a neurodegenerative disease, AD.


Localization (translation) of APP mRNA in dendrites associated with autism, syndrome, alzheimer's dementia and neurodegenerative disease
8) Confidence 0.74 Published 2007 Journal PLoS Biology Section Body Doc Link PMC1808499 Disease Relevance 1.72 Pain Relevance 0
fragments are produced via the cleavage of APP, they begin grouping together, at which point they are believed to produce a neurotoxic effect (Masters et al 2006).
Localization (cleavage) of APP in cleavage
9) Confidence 0.74 Published 2008 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2536544 Disease Relevance 0.70 Pain Relevance 0
The APP/PS1 mouse model used in our study possesses concurrent mutated forms of APP and Presenilin 1 (PS1), both identified separately in human Alzheimer diseases [1].
Localization (forms) of APP associated with disease
10) Confidence 0.73 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2696039 Disease Relevance 0.49 Pain Relevance 0.05
secretion and accumulation of APP C-terminal fragments (CTF) in PS1-/- neurons.
Localization (secretion) of APP in neurons
11) Confidence 0.73 Published 2006 Journal Mol Neurodegener Section Body Doc Link PMC1513131 Disease Relevance 0.09 Pain Relevance 0
In summary, in this review we have tried to give a perspective on the wide variety of interactions between inflammatory mediators and APP secretases.
Localization (secretases) of APP associated with inflammatory mediators
12) Confidence 0.73 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2442055 Disease Relevance 0.57 Pain Relevance 0.74
-secretase occurs via nonamyloidogenic pathway, and a reduced CSF level of sAPP?
Localization (occurs) of APP
13) Confidence 0.73 Published 2010 Journal International Journal of Alzheimer's Disease Section Body Doc Link PMC2915796 Disease Relevance 1.07 Pain Relevance 0
APP is axonally transported and secreted forms of APP (sAPPs) are released from neurons in an activity-driven manner.
Localization (released) of APP in neurons
14) Confidence 0.73 Published 2011 Journal International Journal of Alzheimer's Disease Section Body Doc Link PMC2935165 Disease Relevance 0 Pain Relevance 0.09
APP is axonally transported and secreted forms of APP (sAPPs) are released from neurons in an activity-driven manner.
Localization (secreted) of APP in neurons
15) Confidence 0.73 Published 2011 Journal International Journal of Alzheimer's Disease Section Body Doc Link PMC2935165 Disease Relevance 0 Pain Relevance 0.09
APP is axonally transported and secreted forms of APP (sAPPs) are released from neurons in an activity-driven manner.
Localization (released) of APP in neurons
16) Confidence 0.73 Published 2011 Journal International Journal of Alzheimer's Disease Section Body Doc Link PMC2935165 Disease Relevance 0 Pain Relevance 0.09
In addition, we find that a nuclear receptor, retinoid X receptor alpha (RXRalpha), can regulate Abeta generation and that down-regulation of RXRalpha significantly increases Abeta secretion.
Localization (secretion) of Abeta associated with abeta
17) Confidence 0.72 Published 2009 Journal J. Neurochem. Section Abstract Doc Link 19659691 Disease Relevance 0.68 Pain Relevance 1.01
We also show that (R)-flurbiprofen can interfere with the interaction between RXRalpha and 9-cis-retinoid acid, and that 9-cis-retinoid acid decreases (R)-flurbiprofen's reduction of Abeta secretion.
Localization (secretion) of Abeta associated with abeta
18) Confidence 0.72 Published 2009 Journal J. Neurochem. Section Abstract Doc Link 19659691 Disease Relevance 0.51 Pain Relevance 0.95
Here we find that (R)-flurbiprofen, the R-enantiomer of the racemate NSAID flurbiprofen, can significantly reduce Abeta secretion, but at the same time, increases the level of intracellular Abeta.
Localization (secretion) of Abeta associated with cinod and abeta
19) Confidence 0.72 Published 2009 Journal J. Neurochem. Section Abstract Doc Link 19659691 Disease Relevance 0.77 Pain Relevance 1.03
Lipid raft-localized APP is cleaved by BACE1, whereas APP outside the rafts is a substrate for ?
Localization (localized) of APP
20) Confidence 0.72 Published 2007 Journal Mol Neurodegener Section Body Doc Link PMC2211305 Disease Relevance 0.64 Pain Relevance 0.03

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