INT98178

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Context Info
Confidence 0.65
First Reported 2001
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 32
Total Number 33
Disease Relevance 21.01
Pain Relevance 7.77

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

cytosol (Casp3) peptidase activity (Casp3) mitochondrion (Casp3)
nucleolus (Casp3) nucleus (Casp3) intracellular (Casp3)
Anatomy Link Frequency
neuronal 4
cleavage 4
neurons 3
apoptotic cells 2
ventricles 1
Casp3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Glutamate 890 100.00 Very High Very High Very High
Abeta 12 99.74 Very High Very High Very High
dorsal root ganglion 17 99.08 Very High Very High Very High
allodynia 10 98.96 Very High Very High Very High
Morphine 44 98.74 Very High Very High Very High
Sciatic nerve 6 98.60 Very High Very High Very High
Nucleus accumbens 29 98.40 Very High Very High Very High
antidepressant 15 98.20 Very High Very High Very High
Paracetamol 14 97.86 Very High Very High Very High
antagonist 47 92.68 High High
Disease Link Frequency Relevance Heat
Apoptosis 909 99.78 Very High Very High Very High
Death 603 99.72 Very High Very High Very High
Injury 126 99.42 Very High Very High Very High
Neurodegenerative Disease 100 99.36 Very High Very High Very High
Diabetes Mellitus 296 99.08 Very High Very High Very High
Ganglion Cysts 31 99.08 Very High Very High Very High
Neuropathic Pain 16 98.96 Very High Very High Very High
Toxicity 35 95.52 Very High Very High Very High
Neuroblastoma 4 93.88 High High
Convulsion 263 93.52 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We found a dose-dependent effect of morphine (from 0.01 to 10.0 mg/kg, i.p.) on both the magnitude and the retention of CPP.
Localization (retention) of CPP associated with morphine
1) Confidence 0.65 Published 2009 Journal Behav. Brain Res. Section Abstract Doc Link 19539657 Disease Relevance 0 Pain Relevance 1.53
In the present study, we have determined whether glutamate-induced neuronal apoptosis in primary cortical cells and its inhibition by estrogen, involves changes in caspase-3 protease and whether this process is mediated by Fas receptor and/or mitochondrial signal transduction pathways involving release of cytochrome c.
Localization (protease) of caspase-3 in neuronal associated with glutamate and neurodegenerative disease
2) Confidence 0.59 Published 2005 Journal BMC Neurosci Section Body Doc Link PMC555946 Disease Relevance 0.30 Pain Relevance 0.16
In our study, these p 20 and p11 forms of caspase-3 were not detected in glutamate-induced cell death by immunoblotting analysis with three different kinds of antibodies: i. a polyclonal goat antibody caspase-3 p11 (K-19) against the p11 fragment of caspase-3, ii. a polyclonal rabbit antibody against caspase-3 (H-227) and iii. a monoclonal mouse antibody (E-8) (data not shown with this latter antibody).
Localization (forms) of caspase-3 in E-8 associated with glutamate and death
3) Confidence 0.56 Published 2005 Journal BMC Neurosci Section Body Doc Link PMC555946 Disease Relevance 0.75 Pain Relevance 0.11
We studied the effect of different antidepressants on apoptotic markers, including: cell viability, DNA fragmentation, cytochrome c (Cyt c) release from mitochondria, and caspase-3- like activity.
Localization (release) of caspase-3 associated with antidepressant and apoptosis
4) Confidence 0.43 Published 2005 Journal J. Mol. Neurosci. Section Abstract Doc Link 16055945 Disease Relevance 0.82 Pain Relevance 0.43
Administration of higenamine (bolus, i.p) 1 h prior to I/R-injury significantly decreased the release of cytochrome c, caspase-3 activity, and Bax expression but up-regulated the expression of Bcl-2, HO-1, and HO enzyme activity in the left ventricles, which were inhibited by ZnPP IX, an enzyme inhibitor of HO-1.
Localization (release) of caspase-3 in ventricles associated with injury
5) Confidence 0.42 Published 2006 Journal Apoptosis Section Abstract Doc Link 16703264 Disease Relevance 0.88 Pain Relevance 0.16
Taken together, these findings indicate that the proteolytic cleavage of caspase-3 into active caspase-3 fragments is induced by PTZ and ethanol exposure during pregnancy.


Localization (cleavage) of caspase-3 in cleavage
6) Confidence 0.42 Published 2009 Journal Mol Brain Section Body Doc Link PMC2706809 Disease Relevance 0.57 Pain Relevance 0.04
These observations were further confirmed in primary hippocampal neuronal cells culture by the translocation of cytochrome-c and caspase-3 using confocal microscopy which revealed a diffuse staining pattern of cytochrome-c, suggesting its release from mitochondria (cytochrome-c, green FITC-labeled) along with caspase-3 (TRITC-labeled, red) upon treatments with PTZ, ethanol and PTZ plus ethanol.
Localization (translocation) of caspase-3 in neuronal
7) Confidence 0.42 Published 2009 Journal Mol Brain Section Body Doc Link PMC2706809 Disease Relevance 0.28 Pain Relevance 0.06
Taken together, these findings indicate that the proteolytic cleavage of caspase-3 into active caspase-3 fragments is induced by PTZ and ethanol exposure during pregnancy.


Localization (cleavage) of caspase-3 in cleavage
8) Confidence 0.42 Published 2009 Journal Mol Brain Section Body Doc Link PMC2706809 Disease Relevance 0.58 Pain Relevance 0.04
These observations were further confirmed in primary hippocampal neuronal cells culture by the translocation of cytochrome-c and caspase-3 using confocal microscopy which revealed a diffuse staining pattern of cytochrome-c, suggesting its release from mitochondria (cytochrome-c, green FITC-labeled) along with caspase-3 (TRITC-labeled, red) upon treatments with PTZ, ethanol and PTZ plus ethanol.
Localization (release) of caspase-3 in neuronal
9) Confidence 0.42 Published 2009 Journal Mol Brain Section Body Doc Link PMC2706809 Disease Relevance 0.27 Pain Relevance 0.03
Cytochrome c release and active caspase 3 were markedly increased in nerve from diabetic animals suggesting activation of apoptotic pathway.
Localization (release) of caspase 3 in nerve associated with diabetes mellitus and apoptosis
10) Confidence 0.40 Published 2010 Journal J. Neurochem. Section Abstract Doc Link 19840221 Disease Relevance 1.67 Pain Relevance 0.50
Immunostaining for cleaved caspase-3
Localization (cleaved) of caspase-3
11) Confidence 0.39 Published 2010 Journal Chin Med Section Body Doc Link PMC2984508 Disease Relevance 0.32 Pain Relevance 0.17
Furthermore, activation of calpain precedes that of caspase-3, glutamate-induced LDH release (cell death) and DNA fragmentation in these cells.
Localization (release) of caspase-3 associated with glutamate and death
12) Confidence 0.38 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 1.34 Pain Relevance 0.32
Furthermore, we compared the percentage of neurons injured in the DRG using immunostaining for apoptotic cells and localization of activated caspase 3.
Localization (localization) of caspase 3 in apoptotic cells associated with dorsal root ganglion and apoptosis
13) Confidence 0.38 Published 2009 Journal Eur Spine J Section Abstract Doc Link 19543754 Disease Relevance 3.45 Pain Relevance 1.33
To determine the role of calpain and caspase-3 in primary cortical cells, cells were treated with 1 mM glutamate in the presence or absence of calpain inhibitor (12.5 ?
Spec (determine) Localization (role) of caspase-3 associated with glutamate
14) Confidence 0.36 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 0.67 Pain Relevance 0.32
Effect of estrogens on the activation of calpain and caspase-3
Localization (calpain) of caspase-3
15) Confidence 0.36 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 0.62 Pain Relevance 0.15
In primary cortical cells, glutamate induces activation of calpain, caspase-3 and translocation of AIF from mitochondria to cytosol and nuclei.
Localization (translocation) of caspase-3 associated with glutamate
16) Confidence 0.33 Published 2006 Journal BMC Neurosci Section Abstract Doc Link PMC1526740 Disease Relevance 0.84 Pain Relevance 0.31
exerts potent proapoptotic effects in cardiomyocytes in vitro and in the myocardium in vivo, characterized by the activation of caspase-3 and the cleavage of PARP.
Localization (cleavage) of caspase-3 in cleavage
17) Confidence 0.29 Published 2008 Journal The Open Cardiovascular Medicine Journal Section Body Doc Link PMC2570581 Disease Relevance 0.70 Pain Relevance 0.08
For the localization and distribution of intracellular caspase-3 or caspase-8 protein, immunofluorescence assay was carried out.
Localization (localization) of caspase-3
18) Confidence 0.20 Published 2004 Journal Chin. Med. J. Section Body Doc Link 15265368 Disease Relevance 0.17 Pain Relevance 0
In these conditions, cleaved caspase-3 and p53 clearly labeled damaged neurons as indicated by their co-localization with altered Neurotrace labeling (Additional file 1).
Localization (localization) of caspase-3 in neurons
19) Confidence 0.19 Published 2010 Journal Mol Neurodegener Section Body Doc Link PMC2826326 Disease Relevance 0.23 Pain Relevance 0
In these conditions, cleaved caspase-3 and p53 clearly labeled damaged neurons as indicated by their co-localization with altered Neurotrace labeling (Additional file 1).
Localization (cleaved) of caspase-3 in neurons
20) Confidence 0.19 Published 2010 Journal Mol Neurodegener Section Body Doc Link PMC2826326 Disease Relevance 0.22 Pain Relevance 0

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