INT91511

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Context Info
Confidence 0.67
First Reported 2000
Last Reported 2010
Negated 0
Speculated 1
Reported most in Abstract
Documents 15
Total Number 17
Disease Relevance 14.68
Pain Relevance 3.57

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

transport (CYC1) mitochondrion (CYC1) small molecule metabolic process (CYC1)
cytoplasm (CYC1)
Anatomy Link Frequency
neuronal 2
liver 2
brain 2
apoptotic cell 2
CYC1 (Homo sapiens)
Pain Link Frequency Relevance Heat
aspirin 14 99.98 Very High Very High Very High
cINOD 16 99.80 Very High Very High Very High
opioid receptor 10 97.80 Very High Very High Very High
Endep 5 97.56 Very High Very High Very High
antagonist 3 95.24 Very High Very High Very High
Kinase C 78 90.88 High High
Cannabinoid receptor 2 90.80 High High
fluoxetine 4 90.28 High High
Enkephalin 1 89.92 High High
Spinal cord 2 87.88 High High
Disease Link Frequency Relevance Heat
Apoptosis 119 100.00 Very High Very High Very High
Death 37 100.00 Very High Very High Very High
Cancer 32 100.00 Very High Very High Very High
Hypoxia 12 99.82 Very High Very High Very High
Brain Injury 14 99.72 Very High Very High Very High
Cv Unclassified Under Development 136 98.92 Very High Very High Very High
Toxicity 8 98.64 Very High Very High Very High
Rupture 4 98.08 Very High Very High Very High
Pressure And Volume Under Development 10 97.60 Very High Very High Very High
Parkinson's Disease 234 96.92 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Furthermore, early aspirin-induced cytochrome c release was not affected by the caspase inhibitor Z-VAD x fmk and preceded loss of mitochondrial membrane potential.
Positive_regulation (induced) of Localization (release) of cytochrome c associated with aspirin
1) Confidence 0.67 Published 2000 Journal FEBS Lett. Section Abstract Doc Link 11034327 Disease Relevance 0.42 Pain Relevance 0.35
N-arachidonylglycine causes ROS production and cytochrome c release in liver mitochondria.
Positive_regulation (causes) of Localization (release) of cytochrome c in liver
2) Confidence 0.67 Published 2009 Journal Free Radic. Biol. Med. Section Title Doc Link 19501648 Disease Relevance 0.21 Pain Relevance 0.24
Results show that amitriptyline and tranylcypromine may attenuate the MPP(+) toxicity by suppressing the mitochondrial membrane permeability change that leads to cytochrome c release and subsequent caspase-3 activation.
Positive_regulation (leads) of Localization (release) of cytochrome c associated with toxicity and endep
3) Confidence 0.67 Published 2009 Journal Eur. J. Pharmacol. Section Abstract Doc Link 19135049 Disease Relevance 0.76 Pain Relevance 0.57
The induction of NOXA is therefore essential to override high Mcl-1 levels and allow for the activation of the apoptotic machinery in response to bortezomib.72 Also, NOXA’s interaction with anti-apoptotic members of the Bcl-2 family causes release of cytochrome c into the cytosol, leading to the activation of caspases and induction of apoptosis (Figure 8).73
Positive_regulation (causes) of Localization (release) of cytochrome c associated with apoptosis
4) Confidence 0.49 Published 2010 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2990320 Disease Relevance 0.95 Pain Relevance 0
High glucose also causes a 2 fold increase in Bax expression, which induced cytochrome C release which in turn stimulates apoptosis activating factor, caspase 9 and caspase 3 [41].
Positive_regulation (induced) of Localization (release) of cytochrome C associated with apoptosis
5) Confidence 0.49 Published 2008 Journal The Open Cardiovascular Medicine Journal Section Body Doc Link PMC2570581 Disease Relevance 1.17 Pain Relevance 0.04
Ibuprofen-induced Walker 256 tumor cell death: cytochrome c release from functional mitochondria and enhancement by calcineurin inhibition.
Positive_regulation (enhancement) of Localization (release) of cytochrome c associated with cancer and death
6) Confidence 0.49 Published 2004 Journal Biochem. Pharmacol. Section Title Doc Link 15498510 Disease Relevance 1.09 Pain Relevance 0.10
Ibuprofen-induced Walker 256 tumor cell death: cytochrome c release from functional mitochondria and enhancement by calcineurin inhibition.
Positive_regulation (Ibuprofen-induced) of Localization (release) of cytochrome c associated with cancer and death
7) Confidence 0.49 Published 2004 Journal Biochem. Pharmacol. Section Title Doc Link 15498510 Disease Relevance 1.07 Pain Relevance 0.09
The induction of NOXA is therefore essential to override high Mcl-1 levels and allow for the activation of the apoptotic machinery in response to bortezomib.72 Also, NOXA’s interaction with anti-apoptotic members of the Bcl-2 family causes release of cytochrome c into the cytosol, leading to the activation of caspases and induction of apoptosis (Figure 8).73
Positive_regulation (leading) of Localization (release) of cytochrome c associated with apoptosis
8) Confidence 0.49 Published 2010 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2990320 Disease Relevance 0.96 Pain Relevance 0
The present study utilized a controlled cortical impact model of brain injury to assess the involvement of apoptotic pathways: release of cytochrome c from mitochondria and the activation of caspase-1- and caspase-3-like proteases in the injured cortex at 6, 12 and 24 h post-injury.
Positive_regulation (activation) of Localization (release) of cytochrome c in brain associated with injury, apoptosis and brain injury
9) Confidence 0.49 Published 2002 Journal Brain Res. Section Abstract Doc Link 12213303 Disease Relevance 1.32 Pain Relevance 0.09
Our data suggest that several pro-apoptotic events occur following TBI, however the translocation of cytochrome c itself and/or other events upstream of caspase activation/inhibition may be sufficient to induce neuronal cell death.
Positive_regulation (induce) of Localization (translocation) of cytochrome c in neuronal associated with apoptosis, death and brain injury
10) Confidence 0.49 Published 2002 Journal Brain Res. Section Abstract Doc Link 12213303 Disease Relevance 1.18 Pain Relevance 0.06
Measurements by blot analysis showed that NA-Gly caused a CsA-sensitive cytochrome c release.
Positive_regulation (caused) of Localization (release) of cytochrome c
11) Confidence 0.49 Published 2009 Journal Free Radic. Biol. Med. Section Abstract Doc Link 19501648 Disease Relevance 0.25 Pain Relevance 0.23
This leads to release of pro-apoptotic factors including cytochrome c, that activates caspase 9 and hence caspase 3 [45].
Positive_regulation (leads) of Localization (release) of cytochrome c associated with apoptosis
12) Confidence 0.45 Published 2007 Journal Biochimica et Biophysica Acta Section Body Doc Link PMC2212780 Disease Relevance 0.98 Pain Relevance 0
In addition, it has been shown that the pro-apoptotic factor Bax can translocate to the mitochondria during ischaemia [72] and this, in conjunction with cleaved Bid (tBid), might cause the cytochrome c release observed during prolonged ischaemia [70] despite there being no evidence of MPTP opening [68,98].
Spec (might) Positive_regulation (cause) of Localization (release) of cytochrome c associated with parkinson's disease, cv unclassified under development and apoptosis
13) Confidence 0.45 Published 2007 Journal Biochimica et Biophysica Acta Section Body Doc Link PMC2212780 Disease Relevance 0.94 Pain Relevance 0
An intracellular Ca2+ chelator partially inhibited celecoxib-induced release of cytochrome c from mitochondria, reduced the magnitude of the celecoxib-induced decrease in mitochondrial membrane potential and inhibited celecoxib-induced apoptotic cell death.
Positive_regulation (induced) of Localization (release) of cytochrome c in apoptotic cell associated with apoptosis and death
14) Confidence 0.45 Published 2005 Journal J. Biol. Chem. Section Abstract Doc Link 15987693 Disease Relevance 0.96 Pain Relevance 0.57
The DOR-mediated HPC protection depended on an increase in ERK and Bcl 2 activity, which counteracted the SH-induced increase in p38 MAPK activities and cytochrome c release.
Positive_regulation (increase) of Localization (release) of cytochrome c associated with hypoxia and opioid receptor
15) Confidence 0.45 Published 2005 Journal J. Biol. Chem. Section Abstract Doc Link 15687501 Disease Relevance 0.87 Pain Relevance 0.61
NSAIDs and 5-FU induced the mitochondrial release of cytochrome c as well as caspase-3 and -9 activation, and to a much lesser extent, caspase-8.
Positive_regulation (induced) of Localization (release) of cytochrome c associated with cinod
16) Confidence 0.45 Published 2002 Journal Cancer Res. Section Abstract Doc Link 12414664 Disease Relevance 1.06 Pain Relevance 0.30
Therefore, aspirin-induced apoptosis involves caspase activation through cytochrome c release.
Positive_regulation (activation) of Localization (release) of cytochrome c associated with aspirin and apoptosis
17) Confidence 0.45 Published 2000 Journal FEBS Lett. Section Abstract Doc Link 11034327 Disease Relevance 0.49 Pain Relevance 0.33

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