INT91509

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.78
First Reported 2000
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 39
Total Number 39
Disease Relevance 34.74
Pain Relevance 7.17

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
hepatocytes 1
liver 1
HL-60 1
brain 1
apoptotic cell 1
CYC1 (Homo sapiens)
Pain Link Frequency Relevance Heat
aspirin 69 99.92 Very High Very High Very High
cINOD 90 99.28 Very High Very High Very High
Endep 10 97.38 Very High Very High Very High
opioid receptor 10 97.08 Very High Very High Very High
antagonist 8 93.80 High High
Kinase C 269 90.88 High High
Cannabinoid receptor 3 90.80 High High
fluoxetine 8 89.92 High High
Enkephalin 1 88.48 High High
ischemia 39 88.08 High High
Disease Link Frequency Relevance Heat
Apoptosis 444 100.00 Very High Very High Very High
Death 119 99.96 Very High Very High Very High
Shock 18 99.88 Very High Very High Very High
Brain Injury 32 99.76 Very High Very High Very High
Cancer 93 99.74 Very High Very High Very High
Parkinson's Disease 814 99.32 Very High Very High Very High
Hypoxia 25 99.10 Very High Very High Very High
Cv Unclassified Under Development 492 98.92 Very High Very High Very High
Toxicity 14 98.46 Very High Very High Very High
INFLAMMATION 81 98.44 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.
Localization (release) of cytochrome c associated with aspirin
1) Confidence 0.78 Published 2000 Journal FEBS Lett. Section Abstract Doc Link 11034327 Disease Relevance 0.42 Pain Relevance 0.34
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.
Localization (release) of cytochrome c associated with toxicity and endep
2) Confidence 0.78 Published 2009 Journal Eur. J. Pharmacol. Section Abstract Doc Link 19135049 Disease Relevance 0.76 Pain Relevance 0.57
Experiments are also presented showing that NA-Gly caused a respiration-dependent large ROS production, which seems in turn to be responsible for the inhibition of electron transport activity and cytochrome c release.
Localization (release) of cytochrome c
3) Confidence 0.78 Published 2009 Journal Free Radic. Biol. Med. Section Abstract Doc Link 19501648 Disease Relevance 0.22 Pain Relevance 0.19
N-arachidonylglycine causes ROS production and cytochrome c release in liver mitochondria.
Localization (release) of cytochrome c in liver
4) Confidence 0.78 Published 2009 Journal Free Radic. Biol. Med. Section Title Doc Link 19501648 Disease Relevance 0.21 Pain Relevance 0.24
Measurements by blot analysis showed that NA-Gly caused a CsA-sensitive cytochrome c release.
Localization (release) of cytochrome c
5) Confidence 0.78 Published 2009 Journal Free Radic. Biol. Med. Section Abstract Doc Link 19501648 Disease Relevance 0.25 Pain Relevance 0.22
The intrinsic death pathway is initiated by the mitochondrial release of cytochrome c, a process that is inhibited by anti-apoptotic Bcl-2 proteins.
Localization (release) of cytochrome c associated with apoptosis and death
6) Confidence 0.78 Published 2006 Journal Head Face Med Section Body Doc Link PMC1524725 Disease Relevance 1.07 Pain Relevance 0.06
Indeed, it is well established that survival kinases can block apoptosis by inhibiting cytochrome c release [272].
Localization (release) of cytochrome c associated with apoptosis
7) Confidence 0.78 Published 2007 Journal Biochimica et Biophysica Acta Section Body Doc Link PMC2212780 Disease Relevance 0.89 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].
Localization (release) of cytochrome c associated with parkinson's disease, cv unclassified under development and apoptosis
8) Confidence 0.78 Published 2007 Journal Biochimica et Biophysica Acta Section Body Doc Link PMC2212780 Disease Relevance 0.94 Pain Relevance 0
They might stimulate ROS removal as described above for the ischaemic phase or they could reduce the Bax-induced cytochrome c release.
Localization (release) of cytochrome c
9) Confidence 0.78 Published 2007 Journal Biochimica et Biophysica Acta Section Body Doc Link PMC2212780 Disease Relevance 0.86 Pain Relevance 0
This leads to release of pro-apoptotic factors including cytochrome c, that activates caspase 9 and hence caspase 3 [45].
Localization (release) of cytochrome c associated with apoptosis
10) Confidence 0.78 Published 2007 Journal Biochimica et Biophysica Acta Section Body Doc Link PMC2212780 Disease Relevance 0.97 Pain Relevance 0
Protection from the rise in ROS that accompanies such cytochrome c release could be mediated by survival kinase cascades in two ways.
Localization (release) of cytochrome c
11) Confidence 0.78 Published 2007 Journal Biochimica et Biophysica Acta Section Body Doc Link PMC2212780 Disease Relevance 0.88 Pain Relevance 0
Vitamin E prevents H2O2 – induced apoptosis in remote non-infarcted myocardial cells with prevention of mitochondrial cytochrome C release and activation of caspase 3 [63].
Localization (release) of cytochrome C in myocardial cells associated with apoptosis
12) Confidence 0.78 Published 2008 Journal The Open Cardiovascular Medicine Journal Section Body Doc Link PMC2570581 Disease Relevance 0.78 Pain Relevance 0.08
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].
Localization (release) of cytochrome C associated with apoptosis
13) Confidence 0.78 Published 2008 Journal The Open Cardiovascular Medicine Journal Section Body Doc Link PMC2570581 Disease Relevance 1.16 Pain Relevance 0.04
Moderate hypothermia has been shown to suppress Fas-mediated apoptosis in stored cultured hepatocytes, along with suppression of cytochrome-c release from mitochondria and downstream activation of caspase-7 and caspase-9 [103].
Localization (release) of cytochrome-c in hepatocytes associated with hypothermia and apoptosis
14) Confidence 0.78 Published 2009 Journal Scand J Trauma Resusc Emerg Med Section Body Doc Link PMC2806855 Disease Relevance 1.99 Pain Relevance 0.21
Both compounds prevented the loss of the mitochondrial transmembrane potential, over-expression of Bax, reduction in Bcl-2 level, cytochrome c release, caspase-3 activation, formation of reactive oxygen species and depletion of GSH.
Localization (release) of cytochrome c
15) Confidence 0.78 Published 2009 Journal Eur. J. Pharmacol. Section Abstract Doc Link 19135049 Disease Relevance 0.87 Pain Relevance 0.56
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
Localization (release) of cytochrome c associated with apoptosis
16) Confidence 0.78 Published 2010 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2990320 Disease Relevance 0.95 Pain Relevance 0
Collectively, these results demonstrate cytochrome c release from mitochondria and its redistribution into the cytosol occurs in a time-dependent manner following TBI.
Localization (release) of cytochrome c associated with brain injury
17) Confidence 0.78 Published 2002 Journal Brain Res. Section Abstract Doc Link 12213303 Disease Relevance 1.33 Pain Relevance 0.08
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.
Localization (release) of cytochrome c in brain associated with injury, apoptosis and brain injury
18) Confidence 0.78 Published 2002 Journal Brain Res. Section Abstract Doc Link 12213303 Disease Relevance 1.26 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.
Localization (translocation) of cytochrome c in neuronal associated with apoptosis, death and brain injury
19) Confidence 0.78 Published 2002 Journal Brain Res. Section Abstract Doc Link 12213303 Disease Relevance 1.17 Pain Relevance 0.06
Moreover, we showed that cytochrome c was released during ibuprofen-induced cell death.
Localization (released) of cytochrome c associated with death
20) Confidence 0.78 Published 2004 Journal Biochem. Pharmacol. Section Abstract Doc Link 15498510 Disease Relevance 1.09 Pain Relevance 0.07

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox