INT145929

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Context Info
Confidence 0.60
First Reported 2006
Last Reported 2010
Negated 3
Speculated 1
Reported most in Body
Documents 20
Total Number 21
Disease Relevance 18.12
Pain Relevance 5.35

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

mitochondrion (Bax) endoplasmic reticulum (Bax) intracellular (Bax)
cytoplasm (Bax) cytosol (Bax) cell proliferation (Bax)
Anatomy Link Frequency
brain structures 2
cleavage 1
pore 1
apoptotic cell 1
neuronal 1
Bax (Rattus norvegicus)
Pain Link Frequency Relevance Heat
antagonist 8 100.00 Very High Very High Very High
agonist 3 100.00 Very High Very High Very High
Clonidine 2 100.00 Very High Very High Very High
Morphine 18 99.98 Very High Very High Very High
narcan 2 99.38 Very High Very High Very High
Glutamate 146 99.00 Very High Very High Very High
ischemia 121 98.52 Very High Very High Very High
glial activation 8 98.32 Very High Very High Very High
amygdala 12 97.72 Very High Very High Very High
depression 3 97.56 Very High Very High Very High
Disease Link Frequency Relevance Heat
Apoptosis 493 100.00 Very High Very High Very High
Death 253 100.00 Very High Very High Very High
Stress 169 99.68 Very High Very High Very High
Neurodegenerative Disease 32 99.34 Very High Very High Very High
Injury 118 99.08 Very High Very High Very High
Cancer 102 98.72 Very High Very High Very High
Retina Disease 55 98.52 Very High Very High Very High
Dementia 9 98.40 Very High Very High Very High
Depression 3 97.56 Very High Very High Very High
Pain 9 97.24 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The effects of antagonist of alpha2-adrenoceptors yohimbine and their agonist clonidine on Bax and Bcl-XL mRNA levels in neonatal rat brain were studied.
Regulation (effects) of Bax in brain associated with antagonist, agonist and clonidine
1) Confidence 0.60 Published 2008 Journal Izv. Akad. Nauk. Ser. Biol. Section Abstract Doc Link 18491567 Disease Relevance 0.07 Pain Relevance 0.39
Prolonged morphine application modulates Bax and Hsp70 levels in primary rat neurons.
Regulation (modulates) of Bax in neurons associated with narcan and morphine
2) Confidence 0.59 Published 2008 Journal Neurosci. Lett. Section Title Doc Link 18601975 Disease Relevance 0.45 Pain Relevance 0.94
The selective regulation of Bcl-xl and Bax in hippocampal subfields and of Bcl-2 in the Cg cortex, amygdala, and hypothalamus suggests that these cellular adaptations contribute to the long-term neural plastic adaptations to stress and ADTs in cortical, hypothalamic, and limbic brain structures.
Regulation (regulation) of Bax in brain structures associated with stress and amygdala
3) Confidence 0.49 Published 2008 Journal Neuropsychopharmacology Section Abstract Doc Link 17700647 Disease Relevance 0.84 Pain Relevance 0.58
On the other hand, MnSOD is a major mitochondrial antioxidant enzyme involved in the suppression of apoptosis, via regulation of the Bcl-2 family proteins such as Bcl-2 and Bax (26, 27).
Regulation (regulation) of Bax associated with apoptosis
4) Confidence 0.29 Published 2010 Journal Journal of Korean Medical Science Section Body Doc Link PMC2967004 Disease Relevance 0.91 Pain Relevance 0.03
Fronto-temporal dementia (FTD) is a neurodegenerative disease in which a vascular component is suggested and immunoreactivity of Bax, a proapoptotic protein regulated in part by PACAP/VIP in astrocytes, suggests a role for autoimmunity in the pathology of FTD.44 Astrogliosis in FTD corresponds with SPECT hypoperfusion, suggesting that astrocyte disruption may be related to disturbances of cerebral perfusion in FTD.45 Cognitive dysfunction is associated with reduced cerebral blood flow in different types of dementia.46 Moreover VRS dilatation associated with microvessel abnormality may contribute to the diagnosis of vascular dementias.47 Changes in social behavior occur in cerebrovascular comprise and may result from an FTD-like syndrome.48 Similarly, reduction in cortical blood flow has been identified in CFS patients;49,50 however these findings were not replicated in a study of twins with CFS.51 FTD however is recognized in ALS.91
Regulation (immunoreactivity) of Bax in astrocytes associated with chronic fatigue syndrome, vascular dementia, cognitive disorder, autoimmune disease, dementia, syndrome, neurodegenerative disease and motor neuron diseases
5) Confidence 0.26 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2695238 Disease Relevance 1.67 Pain Relevance 0.14
Our previous studies have shown that depending on the neuronal cell type, glutamate-induced apoptotic cell death was associated with regulation of genes such as Bcl-2, Bax, and/or caspase-3 and mitochondrial cytochrome c.
Regulation (regulation) of Bax in apoptotic cell associated with glutamate, apoptosis and death
6) Confidence 0.26 Published 2006 Journal BMC Neurosci Section Abstract Doc Link PMC1526740 Disease Relevance 0.84 Pain Relevance 0.26
However, taurine treatment inhibited As-induced up-regulation of Bad, Bax and down-regulation of Bcl-2, Bcl-xL.
Regulation (regulation) of Bax
7) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2935368 Disease Relevance 0.71 Pain Relevance 0
It is worth highlighting here that among the genes linked to apoptosis triggered by mitochondrial proteins (Bad and Bid among others) only Bax is regulated.
Regulation (regulated) of Bax associated with apoptosis
8) Confidence 0.25 Published 2008 Journal Molecular Vision Section Body Doc Link PMC2426719 Disease Relevance 1.35 Pain Relevance 0.10
From the results, we identified proapoptotic transcriptional changes, including up regulation of proapoptotic Bax and down regulation of antiapoptotic Bcl-2, using a Western blot assay.
Regulation (regulation) of Bax
9) Confidence 0.24 Published 2010 Journal BMC Complement Altern Med Section Body Doc Link PMC3000377 Disease Relevance 1.28 Pain Relevance 0.17
To determine how morphine affects pro-apoptotic protein Bax and molecular chaperone Hsp70, different concentrations of morphine were examined.
Regulation (affects) of Bax associated with apoptosis and morphine
10) Confidence 0.23 Published 2008 Journal Neurosci. Lett. Section Abstract Doc Link 18601975 Disease Relevance 0.47 Pain Relevance 0.89
At this stage, the Bax per Bcl-2 and Bax:Bcl-xL ratios were not modified.
Neg (not) Regulation (modified) of Bax
11) Confidence 0.22 Published 2009 Journal Molecular Vision Section Abstract Doc Link PMC2765238 Disease Relevance 0.86 Pain Relevance 0.23
The observation that neither the Bax:Bcl-2 nor the Bax:Bcl-xL ratios are regulated at a time when apoptosis is already detectable (3 h) suggests that Bcl-2-related family members are not associated with early cell death following I/R.
Neg (neither) Regulation (regulated) of Bax associated with apoptosis and death
12) Confidence 0.22 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2765238 Disease Relevance 0.56 Pain Relevance 0.07
At the protein level, proapoptotic Bax and Bak were not modulated while Bcl-2 and Bcl-xL were significantly upregulated.
Neg (not) Regulation (modulated) of Bax
13) Confidence 0.22 Published 2009 Journal Molecular Vision Section Abstract Doc Link PMC2765238 Disease Relevance 0.89 Pain Relevance 0.24
The cellular death noted in eleven different cortical regions does not appear to be principally dependent on the apoptosis associated proteins Caspase-3, Bax, Bcl-2, or PARP, but was correlated with glial activation, as indicated by GFAP expression.
Regulation (dependent) of Bax associated with apoptosis, death and glial activation
14) Confidence 0.20 Published 2008 Journal Behav Brain Funct Section Body Doc Link PMC2527299 Disease Relevance 0.95 Pain Relevance 0.49
The present study examined the regulation of the major antiapoptotic (Bcl-2, Bcl-xl) and proapoptotic (Bax) genes by repeated unpredictable stress (an animal model of depression) and antidepressant treatments (ADT).
Spec (examined) Regulation (regulation) of Bax associated with stress, antidepressant and depression
15) Confidence 0.19 Published 2008 Journal Neuropsychopharmacology Section Abstract Doc Link 17700647 Disease Relevance 0.88 Pain Relevance 0.39
Bax, a proapoptotic protein, is a pore-forming cytoplasmic protein which translocates to the outer mitochondrial membrane, influencing its permeability and inducing cytochrome c release from the intermembrane space of the mitochondria into the cytosol, subsequently leading to cell death (Cropton, 2000).
Regulation (influencing) of Bax in pore associated with death
16) Confidence 0.19 Published 2009 Journal Toxicological Sciences Section Body Doc Link PMC2769059 Disease Relevance 0.35 Pain Relevance 0.30
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.
Regulation (regulation) of Bax in cleavage associated with stress, injury, apoptosis and death
17) Confidence 0.15 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2935368 Disease Relevance 0.86 Pain Relevance 0
We observed that NaAsO2 induced up-regulation of pro apoptotic (active non-phospho form of Bad, Bax) and down-regulation of anti apoptotic (active non-phospho form of Bcl-2, Bcl-xL) Bcl-2 family proteins both in vivo and in vitro (Fig. 5A, 5B, 5C, 5D).
Regulation (regulation) of Bax associated with apoptosis
18) Confidence 0.15 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2935368 Disease Relevance 0.91 Pain Relevance 0
Our results also suggest that the ER stress elicited by methapyrilene leads to hepatocellular apoptosis/cell death, as evidenced by the up-regulation of genes involved in apoptosis/cell death, including caspase 9, caspase 11, caspase 12, and BCL-associated X protein.
Regulation (regulation) of BCL-associated X protein associated with stress, apoptosis and death
19) Confidence 0.09 Published 2007 Journal Environ Health Perspect Section Body Doc Link PMC1852695 Disease Relevance 1.44 Pain Relevance 0.05
The upper regulation of Fas and Bax protein was an association phenomenon.
Regulation (regulation) of Bax in upper
20) Confidence 0.03 Published 2006 Journal Journal of Neurochemistry Section Body Doc Link PMC1804119 Disease Relevance 0.78 Pain Relevance 0.03

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