INT111069

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.44
First Reported 2003
Last Reported 2011
Negated 0
Speculated 2
Reported most in Body
Documents 19
Total Number 21
Disease Relevance 7.78
Pain Relevance 5.87

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)
intracellular (Psen1) embryo development (Psen1) protein complex (Psen1)
Anatomy Link Frequency
myocytes 1
neurons 1
brain 1
CHO 1
Psen1 (Mus musculus)
Pain Link Frequency Relevance Heat
bDMF 20 100.00 Very High Very High Very High
addiction 16 100.00 Very High Very High Very High
cINOD 141 98.76 Very High Very High Very High
Inflammation 113 96.84 Very High Very High Very High
cerebral cortex 5 96.44 Very High Very High Very High
Hippocampus 26 95.64 Very High Very High Very High
fibrosis 2 95.28 Very High Very High Very High
antagonist 6 93.40 High High
cytokine 72 87.32 High High
Serotonin 23 85.24 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 140 100.00 Very High Very High Very High
Alzheimer's Dementia 165 99.06 Very High Very High Very High
INFLAMMATION 162 96.84 Very High Very High Very High
Disease 555 96.58 Very High Very High Very High
Fibrosis 2 95.28 Very High Very High Very High
Neurodegenerative Disease 32 92.48 High High
Toxicity 10 90.64 High High
Amyloid Plaque 48 90.52 High High
Sprains And Strains 52 88.88 High High
Death 16 80.84 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Thus, PS1 endoproteolysis, stability and accumulation of PS1 NTF/CTF are regulated by the availability of stoichiometric levels of nicastrin, APH-1 and PEN-2.
Regulation (regulated) of PS1
1) Confidence 0.44 Published 2006 Journal Mol Neurodegener Section Body Doc Link PMC1513131 Disease Relevance 0 Pain Relevance 0
Moreover, we find that presenilin-1 (PS1) mutations, which affect gamma-secretase activity, differentially modulate the cellular A beta 42 response to NSAID treatment.
Regulation (modulate) of PS1 associated with cinod
2) Confidence 0.44 Published 2003 Journal J. Biol. Chem. Section Abstract Doc Link 12805356 Disease Relevance 0.38 Pain Relevance 0.80
Moreover, we find that presenilin-1 (PS1) mutations, which affect gamma-secretase activity, differentially modulate the cellular A beta 42 response to NSAID treatment.
Regulation (affect) of presenilin-1 associated with cinod
3) Confidence 0.44 Published 2003 Journal J. Biol. Chem. Section Abstract Doc Link 12805356 Disease Relevance 0.38 Pain Relevance 0.79
In contrast, expression of the PS1-Delta Exon9 mutation strongly diminishes the A beta 42 response, showing that PS1 mutations can modulate the cellular drug response to NSAID treatment both positively and negatively.
Regulation (modulate) of PS1 associated with cinod
4) Confidence 0.44 Published 2003 Journal J. Biol. Chem. Section Abstract Doc Link 12805356 Disease Relevance 0.33 Pain Relevance 0.85
Moreover, we find that presenilin-1 (PS1) mutations, which affect gamma-secretase activity, differentially modulate the cellular A beta 42 response to NSAID treatment.
Regulation (modulate) of presenilin-1 associated with cinod
5) Confidence 0.44 Published 2003 Journal J. Biol. Chem. Section Abstract Doc Link 12805356 Disease Relevance 0.38 Pain Relevance 0.80
Cardiomyocyte mechanics in myocytes from APP, PS1 and APP/PS1 transgenic murine model
Regulation (model) of PS1 in myocytes associated with targeted disruption
6) Confidence 0.38 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2696039 Disease Relevance 0.48 Pain Relevance 0.05
Finally, the relatively high temporal resolution of the spectral FRET assay (2–3 seconds per image, compared to 3–4 min per image in the FLIM assay) enables near “real time” monitoring of changes in the PS1/?
Regulation (changes) of PS1
7) Confidence 0.33 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2773935 Disease Relevance 0.17 Pain Relevance 0
These data suggest that fenofibrate alters the conformation of the PS1 molecule to favor a “close” PS1 NT-loop and PS1 NT-CT proximity, which correlates with a shift in the APP ?
Regulation (conformation) of PS1
8) Confidence 0.33 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2773935 Disease Relevance 0.05 Pain Relevance 0.03
revealed a wide range of values across the TgAPPsw and PS1/APPsw mouse brain slices, with a 15.3-fold variance for A?
Regulation (values) of PS1 in brain
9) Confidence 0.31 Published 2005 Journal J Neuroinflammation Section Body Doc Link PMC555557 Disease Relevance 0.45 Pain Relevance 0.17
Many FAD pathologic mutations have been reported in the PS1 gene, and transgenic mouse models have been produced by crossbreeding with APP mutant mice to clarify the pathological role of the PS1 mutation on APP mutant mice, such as PS1Tg2576 [13].
Regulation (role) of PS1 associated with targeted disruption and disease
10) Confidence 0.30 Published 2011 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC3018662 Disease Relevance 1.26 Pain Relevance 0.04
production, and presents an allosteric modulation of the “pathogenic” PS1 conformation as an attractive therapeutic strategy.


Regulation (modulation) of PS1
11) Confidence 0.29 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2773935 Disease Relevance 0 Pain Relevance 0
Endoproteolytic processing of PS is a highly conserved and, perhaps, a critical event that regulates the stability of PS1 and possibly the biological activity of PS.
Spec (possibly) Regulation (regulates) of PS1
12) Confidence 0.26 Published 2006 Journal Mol Neurodegener Section Body Doc Link PMC1513131 Disease Relevance 0.06 Pain Relevance 0
These findings demonstrate an adverse effect of PS1 mutations on microglial cells that results in their hyperactivation under pro-inflammatory conditions, which may, together with direct effects of mutant PS1 in neurons, contribute to the neurodegenerative process in AD [104].
Regulation (effect) of PS1 in neurons associated with inflammation, disease and neurodegenerative disease
13) Confidence 0.26 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2442055 Disease Relevance 1.15 Pain Relevance 0.41
and by regulating the presenilin/?
Regulation (regulating) of presenilin
14) Confidence 0.23 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2887037 Disease Relevance 0.71 Pain Relevance 1.04
We reasoned that dilution of the G-PS1-R probe by the wt PS1 would reduce inter-molecular FRET via competitive inhibition of the G-PS1-R/G-PS1-R dimer formation, whereas G-PS1-R intra-molecular FRET would not be affected.
Regulation (affected) of G-PS1
15) Confidence 0.17 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2773935 Disease Relevance 0 Pain Relevance 0.03
peptide forming the dimer and trimer has been confirmed by amino acid sequencing.18 When CHO cells coexpress APP and a FAD-linked mutant PS1 or PS2 gene, oligomeric A?
Regulation (linked) of mutant PS1 in CHO
16) Confidence 0.17 Published 2010 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2938309 Disease Relevance 0.45 Pain Relevance 0
To test whether the ppGpp-mediated negative regulation of activities of pS1 and pS2 in vivo is direct or indirect, we have performed in vitro transcription experiments.
Spec (whether) Regulation (regulation) of pS1
17) Confidence 0.05 Published 2010 Journal Mol Genet Genomics Section Body Doc Link PMC2939334 Disease Relevance 0.07 Pain Relevance 0
S-dependent as it was totally impaired in the rpoS mutant, irrespective of the presence or absence of ppGpp (Fig. 9).Fig. 9Activity of the pS1 promoter in vivo and its dependence on the rpoS gene function.
Regulation (dependence) of pS1 associated with addiction
18) Confidence 0.05 Published 2010 Journal Mol Genet Genomics Section Body Doc Link PMC2939334 Disease Relevance 0.09 Pain Relevance 0.05
Primer extension experiments were performed with primer PS2.rev as described in “Materials and methods”, and the products of the reactions were separated during polyacrylamide gel electrophoresis, with the products of the sequencing reaction (performed using the same primer) run at the same gel (lanes G, A, T and C)

The pS1 and pS2 promoters are negatively regulated by ppGpp in vivo

Regulation (regulated) of pS1
19) Confidence 0.05 Published 2010 Journal Mol Genet Genomics Section Body Doc Link PMC2939334 Disease Relevance 0.08 Pain Relevance 0.04
Since pS1 and pS2 activities appeared to be negatively regulated by ppGpp, we have tested their responses to lack of either one or two major effectors of the stringent response, ppGpp and DksA, in bacteria from stationary phase of growth.
Regulation (regulated) of pS1
20) Confidence 0.05 Published 2010 Journal Mol Genet Genomics Section Body Doc Link PMC2939334 Disease Relevance 0.13 Pain Relevance 0.04

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox