INT286313

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Context Info
Confidence 0.70
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 9
Total Number 12
Disease Relevance 2.26
Pain Relevance 0.76

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
astrocytes 1
cortex 1
neural 1
Psen1 (Mus musculus)
Pain Link Frequency Relevance Heat
Hippocampus 30 99.24 Very High Very High Very High
interneuron 5 96.16 Very High Very High Very High
medulla 5 94.84 High High
Pyramidal cell 5 91.24 High High
addiction 16 81.84 Quite High
imagery 30 57.76 Quite High
cINOD 186 46.32 Quite Low
Inflammatory response 70 34.56 Quite Low
Inflammation 215 30.20 Quite Low
Central nervous system 10 20.24 Low Low
Disease Link Frequency Relevance Heat
Death 23 94.48 High High
Apoptosis 10 94.04 High High
Amyloid Plaque 55 91.52 High High
Targeted Disruption 93 88.64 High High
Disease 435 81.60 Quite High
Brain Injury 15 81.28 Quite High
Hypoxia 25 79.92 Quite High
Sprains And Strains 52 79.76 Quite High
Frontotemporal Dementia 40 70.88 Quite High
Alzheimer's Dementia 78 50.00 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
During mouse development, PS1 mRNA expression is particularly high in neural organs, whereas PS2 is barely expressed.
Transcription (expression) of PS1 in neural
1) Confidence 0.70 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2887037 Disease Relevance 0 Pain Relevance 0.19
production in cells derived from PS1 and PS1/PS2 deficient mice (De Strooper et al., 1998; Zhang et al., 2000) and the absence of A?
Transcription (derived) of PS1
2) Confidence 0.67 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2887037 Disease Relevance 0.85 Pain Relevance 0
production in cells derived from PS1 and PS1/PS2 deficient mice (De Strooper et al., 1998; Zhang et al., 2000) and the absence of A?
Transcription (derived) of PS1
3) Confidence 0.67 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2887037 Disease Relevance 0.86 Pain Relevance 0
Although PS are mainly expressed in neurons, PS1 and PS2 mRNAs are detected at low levels in white matter glial cells and cultured astrocytes (Lee et al., 1996).
Transcription (detected) of PS1 in astrocytes
4) Confidence 0.67 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2887037 Disease Relevance 0.24 Pain Relevance 0.23
By contrast, PS1 and PS2 mRNAs are highly expressed in neurons of the hippocampus and entorhinal cortex in adult mouse brain (Lee et al., 1996).
Transcription (expressed) of PS1 in cortex associated with hippocampus
5) Confidence 0.52 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2887037 Disease Relevance 0 Pain Relevance 0.22
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 ?
Transcription (loop) of PS1
6) Confidence 0.50 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2773935 Disease Relevance 0.05 Pain Relevance 0.03
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 ?
Transcription (loop) of PS1
7) Confidence 0.44 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2773935 Disease Relevance 0.05 Pain Relevance 0.03
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 ?
Transcription (loop) of PS1
8) Confidence 0.44 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2773935 Disease Relevance 0.05 Pain Relevance 0.03
Although DksA alone was not able to inhibit activities of pS1 and pS2 significantly, this protein enhanced the inhibitory effects of ppGpp, when present together with this nucleotide in the reaction mixture (Fig. 12a–d).Fig. 12Effects of DksA and ppGpp on in vitro transcription from the pS1, pS2 (a–d) and ?
Transcription (transcription) of pS1
9) Confidence 0.07 Published 2010 Journal Mol Genet Genomics Section Body Doc Link PMC2939334 Disease Relevance 0 Pain Relevance 0
Positions of transcripts derived from pB, pS1 and pS2 promoters are indicated.
Transcription (derived) of pS1
10) Confidence 0.07 Published 2010 Journal Mol Genet Genomics Section Body Doc Link PMC2939334 Disease Relevance 0 Pain Relevance 0
Positions corresponding to pB, pS1 and pS2 transcription start sites are shown

The pS1 and pS2 promoters are negatively regulated by ppGpp and DksA in vitro

Transcription (transcription) of pS1
11) Confidence 0.07 Published 2010 Journal Mol Genet Genomics Section Body Doc Link PMC2939334 Disease Relevance 0.08 Pain Relevance 0
However, a signal corresponding to the pS1-initiated transcription was evident in the ppGpp0 mutant.
Transcription (transcription) of pS1
12) Confidence 0.05 Published 2010 Journal Mol Genet Genomics Section Body Doc Link PMC2939334 Disease Relevance 0.07 Pain Relevance 0.04

General Comments

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