INT88919

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Context Info
Confidence 0.70
First Reported 2000
Last Reported 2011
Negated 0
Speculated 0
Reported most in Abstract
Documents 39
Total Number 39
Disease Relevance 28.64
Pain Relevance 8.18

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

cytosol (Casp9) peptidase activity (Casp9) mitochondrion (Casp9)
aging (Casp9) nucleus (Casp9) cytoplasm (Casp9)
Anatomy Link Frequency
poly 2
cerebral cortex 2
hepatocytes 1
RVLM 1
cleavage 1
Casp9 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
qutenza 18 99.68 Very High Very High Very High
Paracetamol 21 98.82 Very High Very High Very High
Clonidine 21 98.76 Very High Very High Very High
cerebral cortex 20 98.76 Very High Very High Very High
Rostral ventrolateral medulla 7 98.08 Very High Very High Very High
withdrawal 15 97.72 Very High Very High Very High
methadone 12 97.22 Very High Very High Very High
Inflammation 45 96.40 Very High Very High Very High
Arthritis 26 90.56 High High
antagonist 16 89.28 High High
Disease Link Frequency Relevance Heat
Hypoxia 66 99.82 Very High Very High Very High
Cerebral Hypoxia 12 99.76 Very High Very High Very High
Apoptosis 869 99.74 Very High Very High Very High
Death 238 99.36 Very High Very High Very High
Toxicity 62 99.08 Very High Very High Very High
Leukemia 20 97.94 Very High Very High Very High
Stress 91 97.90 Very High Very High Very High
Injury 38 97.30 Very High Very High Very High
Shock 4 96.48 Very High Very High Very High
INFLAMMATION 61 96.40 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Acetaminophen maintained mitochondrial cytochrome c content and reduced activation of caspase-9 and incidence of apoptosis.
Positive_regulation (activation) of caspase-9 associated with paracetamol and apoptosis
1) Confidence 0.70 Published 2010 Journal Brain Res. Section Abstract Doc Link 20079345 Disease Relevance 1.22 Pain Relevance 1.02
Firstly, there is a downstream caspase cascade that occurs with the activation of the Casp9 (caspase-9) gene, an initiator of proteinas through damage of mitochondria [22].
Positive_regulation (activation) of caspase-9
2) Confidence 0.67 Published 2010 Journal Korean Journal of Anesthesiology Section Body Doc Link PMC2872860 Disease Relevance 0.95 Pain Relevance 0.07
Our experimental evidence suggests that APAP-induced nephro-toxicity is a caspase-dependent process that involves activation of caspase-9 and caspase-3 in the absence of cytosolic cytochrome C release.
Positive_regulation (activation) of caspase-9 associated with toxicity and paracetamol
3) Confidence 0.67 Published 2010 Journal Toxicology Section Abstract Doc Link 19922764 Disease Relevance 0.62 Pain Relevance 0.61
Firstly, there is a downstream caspase cascade that occurs with the activation of the Casp9 (caspase-9) gene, an initiator of proteinas through damage of mitochondria [22].
Positive_regulation (activation) of Casp9
4) Confidence 0.60 Published 2010 Journal Korean Journal of Anesthesiology Section Body Doc Link PMC2872860 Disease Relevance 0.95 Pain Relevance 0.07
Neonatal capsaicin administration induced caspase-9-immunoreactivity (ir) and -3-ir.
Positive_regulation (induced) of caspase-9-immunoreactivity associated with qutenza
5) Confidence 0.41 Published 2005 Journal Arch. Histol. Cytol. Section Abstract Doc Link 16477149 Disease Relevance 0.15 Pain Relevance 0.59
This increase in caspase-9 activity was blocked by isoflurane at 1.6 MAC and halothane at 1.2 MAC.
Positive_regulation (increase) of caspase-9
6) Confidence 0.41 Published 2000 Journal Anesthesiology Section Body Doc Link 10861165 Disease Relevance 0 Pain Relevance 0
NE treatment increased caspase-9 activity to 197 +/- 62% over control myocytes (P < 0.0001), whereas no caspase-8 activation was detectable.
Positive_regulation (increased) of caspase-9 in myocytes
7) Confidence 0.41 Published 2000 Journal Anesthesiology Section Body Doc Link 10861165 Disease Relevance 0.05 Pain Relevance 0
Extracts from ouabain-treated hearts had an elevation of cytochrome c in cytosol and a corresponding decrease in mitochondria; this release of cytochrome c provoked activation of caspase-9 and -3.
Positive_regulation (activation) of caspase-9 in hearts
8) Confidence 0.35 Published 2007 Journal Eur. J. Pharmacol. Section Abstract Doc Link 17466970 Disease Relevance 0.30 Pain Relevance 0.06
Caspase-9 activity (nmoles/mg protein/h) was 0.548 +/- 0.0642 in Nx and increased to 0.808 +/- 0.080 (P < 0.05 vs.
Positive_regulation (increased) of Caspase-9
9) Confidence 0.34 Published 2007 Journal Neurochem. Res. Section Abstract Doc Link 17268855 Disease Relevance 0.63 Pain Relevance 0.32
Mechanism of activation of caspase-9 and caspase-3 during hypoxia in the cerebral cortex of newborn piglets: the role of nuclear Ca2+ -influx.
Positive_regulation (activation) of caspase-9 in cerebral cortex associated with hypoxia and cerebral cortex
10) Confidence 0.34 Published 2007 Journal Neurochem. Res. Section Title Doc Link 17268855 Disease Relevance 0.64 Pain Relevance 0.27
The present study tests the hypothesis that inhibiting nuclear Ca2+ -influx by pretreatment with clonidine, an inhibitor of high affinity Ca2+ -ATPase, will prevent the hypoxia-induced increase in caspase-9 and caspase-3 activity in the cerebral cortex of newborn piglets.
Positive_regulation (increase) of caspase-9 in cerebral cortex associated with hypoxia, cerebral cortex and clonidine
11) Confidence 0.34 Published 2007 Journal Neurochem. Res. Section Abstract Doc Link 17268855 Disease Relevance 0.68 Pain Relevance 0.32
The data demonstrate that clonidine administration prior to hypoxia prevents the hypoxia-induced increase in the activity of caspase-9 and caspase-3.
Positive_regulation (increase) of caspase-9 associated with hypoxia and clonidine
12) Confidence 0.34 Published 2007 Journal Neurochem. Res. Section Abstract Doc Link 17268855 Disease Relevance 0.45 Pain Relevance 0.22
We conclude that the high afinity Ca2+ -ATPase-dependent increased nuclear Ca2+ during hypoxia results in increased caspase-9 and caspase-3 activity.
Positive_regulation (increased) of caspase-9 associated with hypoxia
13) Confidence 0.34 Published 2007 Journal Neurochem. Res. Section Abstract Doc Link 17268855 Disease Relevance 0.47 Pain Relevance 0.18
CPS-induced apoptosis involved intracellular free calcium (Ca2+) influx, phosphatidylserine exposure, mitochondrial permeability transmembrane pore (PTP) opening and mitochondrial transmembrane potential (Delta Psi m) dissipation leading to cytochrome c release, activation of caspase-9 and -3 and oligonucleosomal DNA fragmentation.
Positive_regulation (activation) of caspase-9 and -3 in pore associated with qutenza and apoptosis
14) Confidence 0.32 Published 2004 Journal Cell Death Differ. Section Abstract Doc Link 15459754 Disease Relevance 0.58 Pain Relevance 0.66
In previous studies, we have shown that cerebral hypoxia results in increased activity of caspase-9, the initiator caspase, and caspase-3, the executioner of programmed cell death.
Positive_regulation (increased) of caspase-9 associated with cerebral hypoxia and apoptosis
15) Confidence 0.23 Published 2007 Journal Neurochem. Res. Section Abstract Doc Link 17268855 Disease Relevance 0.53 Pain Relevance 0.18
LPS also induced nitric oxide (NO) and superoxide (O(2)(-)) production, depressed mitochondrial Complex I and IV activity, promoted the release of cytochrome c from mitochondria to cytosol, upregulated the cytosolic expression of activated caspase-9 and -3, or increased caspase-3 enzyme activity in the RVLM.
Positive_regulation (activated) of caspase-9 and -3 in RVLM associated with rostral ventrolateral medulla
16) Confidence 0.22 Published 2005 Journal Free Radic. Biol. Med. Section Abstract Doc Link 16085179 Disease Relevance 0.83 Pain Relevance 0.47
Methadone inhibited proliferation in leukemia cells and induced cell death through apoptosis induction and activated apoptosis pathways through the activation of caspase-9 and caspase-3, down-regulation of Bcl-x(L) and X chromosome-linked inhibitor of apoptosis, and cleavage of poly(ADP-ribose) polymerase.
Positive_regulation (activation) of caspase-9 in poly associated with leukemia, methadone, apoptosis and death
17) Confidence 0.16 Published 2008 Journal Cancer Res. Section Abstract Doc Link 18676827 Disease Relevance 1.58 Pain Relevance 0.99
It results in the mitochondrial release of cytochrome C which activates initiator caspase-9 [28], [29] and was shown to contribute to cell death of HEK293 (human kidney cell line) upon Fe(III)-salen treatment [22] and also in the present study for SKOV-3 cells upon Fe(III)-salophene treatment.
Positive_regulation (activates) of caspase-9 in kidney associated with death
18) Confidence 0.15 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2386551 Disease Relevance 0.91 Pain Relevance 0
Treatment with 1.25 µM Fe-SP revealed a similar result, with some activation of caspase-9, and -3, and inactivation of PARP-1 while the activation of caspase-8 was as strong as observed for 2.5 µM Fe-SP.
Positive_regulation (activation) of caspase-9
19) Confidence 0.15 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2386551 Disease Relevance 0.56 Pain Relevance 0
Fe-SP treatment led to the activation of markers of the extrinsic (Caspase-8) and intrinsic (Caspase-9) pathway of apoptosis as well as of executioner Caspase-3 while PARP-1 was deactivated.
Positive_regulation (activation) of Caspase-9 associated with apoptosis
20) Confidence 0.15 Published 2008 Journal PLoS ONE Section Abstract Doc Link PMC2386551 Disease Relevance 0.65 Pain Relevance 0

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