INT137634

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Context Info
Confidence 0.80
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 17
Total Number 17
Disease Relevance 11.80
Pain Relevance 3.45

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
neuronal 1
liver 1
hepatocytes 1
AsPC-1 1
BxPC-3 1
Aifm1 (Mus musculus)
Pain Link Frequency Relevance Heat
Paracetamol 32 98.76 Very High Very High Very High
Glutamate 144 98.26 Very High Very High Very High
qutenza 24 97.88 Very High Very High Very High
withdrawal 1 97.52 Very High Very High Very High
antagonist 3 76.32 Quite High
addiction 7 59.80 Quite High
alcohol 14 50.00 Quite Low
agonist 1 48.36 Quite Low
ischemia 4 45.48 Quite Low
Thoracotomy 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Death 177 100.00 Very High Very High Very High
Parkinson's Disease 20 99.72 Very High Very High Very High
Apoptosis 514 99.64 Very High Very High Very High
Stress 9 99.48 Very High Very High Very High
Cancer 307 93.88 High High
Hepatotoxicity 4 93.76 High High
Lung Cancer 60 88.56 High High
Non-small-cell Lung Cancer 96 87.40 High High
Prostate Cancer 34 84.16 Quite High
Pancreatic Cancer 14 78.64 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Using immunofluorescence microscopy, it was shown that in primary cultured mouse hepatocytes, endonuclease G and AIF translocated to the nucleus between 3 and 6 h after exposure to 5 mM AAP.
Localization (translocated) of AIF in hepatocytes associated with paracetamol
1) Confidence 0.80 Published 2006 Journal Toxicol. Sci. Section Abstract Doc Link 16896059 Disease Relevance 0.50 Pain Relevance 0.41
The translocation of AIF and endonuclease G correlated with mitochondrial dysfunction as indicated by the progressive loss of the mitochondrial membrane potential (measured with the JC-1 assay) and the appearance of nuclear DNA fragments in the cytosol (determined by an anti-histone ELISA).
Localization (translocation) of AIF associated with parkinson's disease
2) Confidence 0.80 Published 2006 Journal Toxicol. Sci. Section Abstract Doc Link 16896059 Disease Relevance 0.51 Pain Relevance 0.43
The data support the conclusion that endonuclease G and AIF translocate to the nucleus in response to AAP-induced mitochondrial dysfunction and may be responsible, at least in part, for the initial DNA fragmentation during AAP hepatotoxicity.
Localization (translocate) of AIF in nucleus associated with parkinson's disease, paracetamol and hepatotoxicity
3) Confidence 0.80 Published 2006 Journal Toxicol. Sci. Section Abstract Doc Link 16896059 Disease Relevance 0.52 Pain Relevance 0.40
Pretreatment with 20mM N-acetylcysteine prevented mitochondrial dysfunction, the nuclear translocation of endonuclease G and AIF, and the nuclear DNA fragmentation.
Localization (translocation) of AIF associated with parkinson's disease
4) Confidence 0.80 Published 2006 Journal Toxicol. Sci. Section Abstract Doc Link 16896059 Disease Relevance 0.39 Pain Relevance 0.39
Since in HT22 cells, glutamate also induced DNA laddering, mitochondrial proteins such as apoptosis inducing factor (AIF) and endonuclease G (Endo G) released in response to death signals may also play a role in the HT22 neuronal cell line [13].
Localization (released) of AIF in neuronal associated with glutamate, apoptosis and death
5) Confidence 0.78 Published 2005 Journal BMC Neurosci Section Body Doc Link PMC555946 Disease Relevance 0.80 Pain Relevance 0.22
CONCLUSIONS: The results indicate that WLP-S-10 is a novel potential compound against acetaminophen-induced acute liver failure in mice, and its active mechanism is mainly related to protection against necrosis and apoptosis of hepatocytes through inhibition of mitochondrial energy (ATP) depletion and AIF and cytochrome C release.


Localization (release) of AIF in liver
6) Confidence 0.74 Published 2008 Journal Liver Int. Section Body Doc Link 18435715 Disease Relevance 0 Pain Relevance 0
WLP-S-10 inhibited mitochondrial swelling, breakdown of membrane potential and depletion of mitochondrial ATP, and also reduced release of cytochrome C and AIF from mitochondria induced by acetaminophen.
Localization (release) of AIF
7) Confidence 0.74 Published 2008 Journal Liver Int. Section Body Doc Link 18435715 Disease Relevance 0 Pain Relevance 0
Exposure of AsPC-1 and BxPC-3 cells to capsaicin was also associated with increased expression of Bax, down-regulation of bcl-2, survivin and significant release of cytochrome c and AIF in the cytosol.
Localization (release) of AIF in BxPC-3 associated with qutenza
8) Confidence 0.57 Published 2008 Journal Apoptosis Section Abstract Doc Link 19002586 Disease Relevance 0.95 Pain Relevance 0.73
AIF, another important factor normally localizes to the mitochondrial inter-membrane space, plays a critical role in the caspase-independent apoptosis [44].
Localization (localizes) of AIF associated with apoptosis
9) Confidence 0.41 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2807457 Disease Relevance 0.84 Pain Relevance 0
In the context of enhanced mitochondria triggered cell death due to disrupted mitochondrial transmembrane potential we detected the release of cytochrome-c, AIF and Smac/Diabolo into the cytoplasm, decreased levels of anti-apoptotoc c-IAP1 and c-IAP2 but unchanged levels of XIAP.
Localization (release) of AIF associated with death
10) Confidence 0.29 Published 2006 Journal J Carcinog Section Body Doc Link PMC1665446 Disease Relevance 0.92 Pain Relevance 0
We investigated the activation of several central apoptosis regulators, such as caspase-8 and its substrate Bid, caspase-9 and caspase-3, along with crucial biochemical parameters such as mitochondrial integrity and release of cytochrome-c, Smac/Diabolo and AIF into the cytoplasm.
Localization (release) of AIF associated with apoptosis
11) Confidence 0.29 Published 2006 Journal J Carcinog Section Body Doc Link PMC1665446 Disease Relevance 1.17 Pain Relevance 0
Combination therapy significantly increased changes in MTP and the release of cyto-c, AIF and Smac/Diabolo into the cytoplasm.
Localization (release) of AIF
12) Confidence 0.26 Published 2006 Journal J Carcinog Section Abstract Doc Link PMC1665446 Disease Relevance 1.16 Pain Relevance 0
These results were confirmed by the demonstration of cytochrome-c, Smac/Diabolo and AIF release from mitochondria into the cytosol, as detected by Western blot analyses of cytosolic proteins.
Localization (release) of AIF
13) Confidence 0.26 Published 2006 Journal J Carcinog Section Body Doc Link PMC1665446 Disease Relevance 0.41 Pain Relevance 0.03
Noteworthy in this regard is the release of the caspase-independent cell death effector AIF into the cytoplasm, which likely helps to explain why in this study combined chemotherapy induced apotosis was partially inhibited by the broad spectrum caspase-inhibitor zVAD.
Localization (release) of AIF associated with death
14) Confidence 0.26 Published 2006 Journal J Carcinog Section Body Doc Link PMC1665446 Disease Relevance 0.83 Pain Relevance 0
Upon withdrawal of survival factors BAD becomes dephosphorylated, shifts the balance of pro- and anti-apoptotic Bcl proteins that triggers release of cytochrome c, SMAC and AIF from mitochondria and subsequently leads to apoptosis [12].
Localization (release) of AIF associated with apoptosis and withdrawal
15) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2704953 Disease Relevance 1.36 Pain Relevance 0.09
Exposure of AsPC-1 and BxPC-3 cells to capsaicin was also associated with increased expression of Bax, down-regulation of bcl-2, survivin and significant release of cytochrome c and AIF in the cytosol.
Localization (release) of AIF in AsPC-1 associated with qutenza
16) Confidence 0.19 Published 2008 Journal Apoptosis Section Abstract Doc Link 19002586 Disease Relevance 0.95 Pain Relevance 0.73
In the cytosolic fractions of combination chemotherapy-exposed KNS62 cells there was a significantly higher release of cytochrome-c, Smac/Diabolo and AIF into the cytosole compared to single agent (gemcitabine or phenylbutyrate) therapy (Fig. 4b).
Localization (release) of AIF
17) Confidence 0.11 Published 2006 Journal J Carcinog Section Body Doc Link PMC1665446 Disease Relevance 0.50 Pain Relevance 0.03

General Comments

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