INT121964

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Context Info
Confidence 0.32
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 8
Total Number 8
Disease Relevance 5.52
Pain Relevance 1.73

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
cerebral cortex 2
cleavage 2
pore 2
hearts 2
Casp9 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Clonidine 9 99.08 Very High Very High Very High
cerebral cortex 8 98.76 Very High Very High Very High
qutenza 10 95.46 Very High Very High Very High
antagonist 1 89.28 High High
Morphine 1 70.52 Quite High
Glutamate 144 69.80 Quite High
anesthesia 3 57.56 Quite High
Kinase C 21 5.00 Very Low Very Low Very Low
Analgesic 1 5.00 Very Low Very Low Very Low
Nerve growth factor 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Hypoxia 29 100.00 Very High Very High Very High
Apoptosis 161 99.48 Very High Very High Very High
Stress 21 98.44 Very High Very High Very High
Injury 5 97.84 Very High Very High Very High
Death 86 97.36 Very High Very High Very High
Necrosis 6 89.20 High High
Cerebral Hypoxia 4 88.28 High High
Adenocarcinoma 10 87.52 High High
Body Weight 41 84.32 Quite High
Ovarian Cancer 32 76.08 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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 (leading) of Positive_regulation (activation) of caspase-9 and -3 in pore associated with qutenza and apoptosis
1) Confidence 0.32 Published 2004 Journal Cell Death Differ. Section Abstract Doc Link 15459754 Disease Relevance 0.58 Pain Relevance 0.67
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 (provoked) of Positive_regulation (activation) of caspase-9 in hearts
2) Confidence 0.25 Published 2007 Journal Eur. J. Pharmacol. Section Abstract Doc Link 17466970 Disease Relevance 0.30 Pain Relevance 0.06
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 (hypoxia-induced) of Positive_regulation (increase) of caspase-9 in cerebral cortex associated with hypoxia, cerebral cortex and clonidine
3) Confidence 0.24 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 (hypoxia-induced) of Positive_regulation (increase) of caspase-9 associated with hypoxia and clonidine
4) Confidence 0.24 Published 2007 Journal Neurochem. Res. Section Abstract Doc Link 17268855 Disease Relevance 0.45 Pain Relevance 0.22
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 (led) of Positive_regulation (activation) of Caspase-9 associated with apoptosis
5) Confidence 0.10 Published 2008 Journal PLoS ONE Section Abstract Doc Link PMC2386551 Disease Relevance 0.65 Pain Relevance 0
Cytosolic cytochrome c binds to Apaf-1 in the presence of dATP and this leads to the recruitment and activation of caspase-9 and subsequent activation of caspase-3 [23,25].
Positive_regulation (leads) of Positive_regulation (activation) of caspase-9
6) Confidence 0.06 Published 2005 Journal BMC Neurosci Section Body Doc Link PMC555946 Disease Relevance 0.50 Pain Relevance 0.20
As caused mitochondrial injury by increased oxidative stress and reciprocal regulation of Bcl-2, Bcl-xL/Bad, Bax, Bim in association with increased level of Apaf-1, activation of caspase 9/3, cleavage of PARP protein and ultimately led to apoptotic cell death.
Positive_regulation (increased) of Positive_regulation (activation) of caspase 9 in cleavage associated with stress, injury, apoptosis and death
7) Confidence 0.06 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2935368 Disease Relevance 0.85 Pain Relevance 0
We propose that during hypoxia the increased ratio of (pro-apoptotic Bad and Bax/anti-apoptotic Bcl-xl and Bcl-2) in all the three compartments, will lead to altered mitochondrial and nuclear membrane permeability as well as caspase-9 activation in the cytosolic compartment.
Positive_regulation (lead) of Positive_regulation (activation) of caspase-9 associated with hypoxia and apoptosis
8) Confidence 0.02 Published 2008 Journal Neurochem. Res. Section Abstract Doc Link 18293086 Disease Relevance 1.51 Pain Relevance 0.26

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