INT164540

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Context Info
Confidence 0.46
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 15
Total Number 17
Disease Relevance 13.87
Pain Relevance 3.65

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

cytosol (Aifm1) mitochondrion (Aifm1) oxidoreductase activity (Aifm1)
nucleus (Aifm1) DNA binding (Aifm1) cytoplasm (Aifm1)
Anatomy Link Frequency
nucleus 2
neuronal 1
apoptotic cell 1
Aifm1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Glutamate 1731 99.08 Very High Very High Very High
Paracetamol 16 97.96 Very High Very High Very High
antagonist 12 68.72 Quite High
Neurotransmitter 36 67.80 Quite High
excitatory amino acid 12 67.12 Quite High
Glutamate receptor 30 52.16 Quite High
ischemia 36 40.04 Quite Low
cytokine 3 27.88 Quite Low
Neuritis 12 25.40 Quite Low
imagery 6 22.80 Low Low
Disease Link Frequency Relevance Heat
Death 1093 99.74 Very High Very High Very High
Apoptosis 1270 99.64 Very High Very High Very High
Stress 21 96.64 Very High Very High Very High
Parkinson's Disease 12 95.72 Very High Very High Very High
Toxicity 40 95.60 Very High Very High Very High
Neurodegenerative Disease 135 91.36 High High
Injury 43 87.56 High High
Necrosis 15 86.96 High High
Osteoporosis 12 83.20 Quite High
Hypoxia 18 77.60 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In the present paper, we show that apoptosis inducing factor (AIF), normally confined in the mitochondria, is also released into the cytosol and nuclei in primary cortical cells undergoing apoptosis and upregulation of AIF also occurs in HT22 cells after glutamate treatment.
Localization (released) of AIF associated with glutamate and apoptosis
1) Confidence 0.46 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 0.84 Pain Relevance 0.16
Based on these studies, glutamate-induced overexpression of AIF in HT22 cells might also trigger AIF release or translocation from the mitochondria into the cytosol and nuclei.
Localization (release) of AIF associated with glutamate
2) Confidence 0.43 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 0.61 Pain Relevance 0.09
In primary cortical cells, glutamate induces activation of calpain, caspase-3 and translocation of AIF from mitochondria to cytosol and nuclei.
Localization (translocation) of AIF associated with glutamate
3) Confidence 0.40 Published 2006 Journal BMC Neurosci Section Abstract Doc Link PMC1526740 Disease Relevance 0.83 Pain Relevance 0.31
In contrast, in HT22 cells, only the activation of calpain and upregulation and translocation of AIF occurred.
Localization (translocation) of AIF
4) Confidence 0.40 Published 2006 Journal BMC Neurosci Section Abstract Doc Link PMC1526740 Disease Relevance 0.92 Pain Relevance 0.30
These results indicate that AIF protein is released or translocates from mitochondria into cytosol and nuclei in primary cortical cells undergoing apoptotic cell death following exposure to glutamate.
Localization (released) of AIF protein in apoptotic cell associated with glutamate, apoptosis and death
5) Confidence 0.40 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 0.83 Pain Relevance 0.26
Whether translocation of AIF is involved in this process requires further study.
Localization (translocation) of AIF
6) Confidence 0.40 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 0.38 Pain Relevance 0.36
Glutamate-induced apoptotic cell death in neuronal cells was associated with characteristic DNA fragmentation, morphological changes, activation of calpain and caspase-3 as well as the upregulation and/or translocation of AIF from mitochondria into cytosol and nuclei.
Localization (translocation) of AIF in neuronal associated with glutamate, apoptosis and death
7) Confidence 0.40 Published 2006 Journal BMC Neurosci Section Abstract Doc Link PMC1526740 Disease Relevance 0.80 Pain Relevance 0.26
Furthermore, a reduction in mitochondrial transmembrane potential has been reported to accompany AIF release and early apoptosis [15,16].
Localization (release) of AIF associated with apoptosis
8) Confidence 0.40 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 1.05 Pain Relevance 0.13
Taken together with previous studies, our data indicate that glutamate exerts its toxic action through two parallel pathways: a caspase-dependent pathway mediated by caspase-3, the final apoptotic effector, and a caspase-3 independent apoptotic pathway involving the upregulation of AIF and/or mitochondrial AIF release as well as calpain-modulated effects (cell death).
Localization (release) of AIF associated with glutamate, apoptosis and death
9) Confidence 0.37 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 0.83 Pain Relevance 0.16
, induces AIF release from the mitochondria and causes apoptosis.
Localization (release) of AIF associated with apoptosis
10) Confidence 0.37 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 0.55 Pain Relevance 0.11
Measurement of AIF translocation
Localization (translocation) of AIF
11) Confidence 0.37 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 0.16 Pain Relevance 0.07
The release of AIF in excitotoxicity and apoptosis is likewise inhibited by Bcl-2 [10,17], suggesting that the activation of BH3-only proteins may also be required to relieve a Bcl-2 inhibition of AIF release.
Localization (release) of AIF associated with apoptosis
12) Confidence 0.37 Published 2007 Journal BMC Cell Biol Section Body Doc Link PMC1808451 Disease Relevance 1.15 Pain Relevance 0.05
When apoptotic cell death is induced, AIF translocates through the outer mitochondrial membrane to the cytosol and nucleus, where it leads to nuclear chromatin condensation and a large-scale DNA fragmentation (high molecular weight DNA fragments) and apoptosis in a caspase-independent manner [10,11].
Localization (translocates) of AIF in nucleus associated with apoptosis and death
13) Confidence 0.35 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 0.72 Pain Relevance 0.06
In the absence of caspase activation MOMP may activate alternative cell death pathways that include ATP depletion and increased ROS production subsequent to cyt-C release, as well as the release of AIF [7,9,38-40].
Localization (release) of AIF associated with death
14) Confidence 0.32 Published 2007 Journal BMC Cell Biol Section Body Doc Link PMC1808451 Disease Relevance 0.87 Pain Relevance 0
The release of AIF in excitotoxicity and apoptosis is likewise inhibited by Bcl-2 [10,17], suggesting that the activation of BH3-only proteins may also be required to relieve a Bcl-2 inhibition of AIF release.
Localization (release) of AIF associated with apoptosis
15) Confidence 0.32 Published 2007 Journal BMC Cell Biol Section Body Doc Link PMC1808451 Disease Relevance 1.19 Pain Relevance 0.07
In addition, pharmacological inhibition of AIF translocation may effectively protect against or at least delay acetaminophen-induced programmed cell death.
Localization (translocation) of AIF associated with paracetamol and apoptosis
16) Confidence 0.10 Published 2010 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 19931551 Disease Relevance 1.10 Pain Relevance 0.62
However, BGP-15 prevented AIF mitochondria-to-nucleus translocation and mitochondrial depolarization.
Localization (translocation) of AIF in nucleus
17) Confidence 0.09 Published 2010 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 19931551 Disease Relevance 1.04 Pain Relevance 0.64

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