INT101858

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Context Info
Confidence 0.57
First Reported 2002
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 25
Total Number 26
Disease Relevance 23.77
Pain Relevance 4.16

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

lipid binding (BAX) cytosol (BAX) mitochondrion (BAX)
endoplasmic reticulum (BAX) nucleus (BAX) cytoplasm (BAX)
Anatomy Link Frequency
liver 1
hepatocytes 1
neurons 1
BAX (Homo sapiens)
Pain Link Frequency Relevance Heat
Morphine 8 99.98 Very High Very High Very High
antagonist 25 99.96 Very High Very High Very High
cINOD 46 99.60 Very High Very High Very High
agonist 16 99.50 Very High Very High Very High
diclofenac 12 98.24 Very High Very High Very High
qutenza 12 96.04 Very High Very High Very High
aspirin 12 93.04 High High
metalloproteinase 68 92.24 High High
addiction 8 90.12 High High
Inflammation 55 88.76 High High
Disease Link Frequency Relevance Heat
Apoptosis 819 100.00 Very High Very High Very High
Colon Cancer 114 99.68 Very High Very High Very High
Death 192 99.54 Very High Very High Very High
INFLAMMATION 76 99.32 Very High Very High Very High
Injury 37 98.78 Very High Very High Very High
Cancer 605 96.72 Very High Very High Very High
Arthritis 3 96.28 Very High Very High Very High
Shock 16 95.76 Very High Very High Very High
Disease 113 93.44 High High
Stress 34 92.24 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Morphine downregulates proapoptotic factor Bax levels in cultured human neurons.
Negative_regulation (downregulates) of Bax in neurons associated with morphine
1) Confidence 0.57 Published 2008 Journal Neuroreport Section Abstract Doc Link 18849879 Disease Relevance 0.26 Pain Relevance 0.80
In this system, the NSAID-provoked cell death was associated with a downregulation of Bax-antagonist Bcl-XL.
Negative_regulation (downregulation) of Bax associated with antagonist, cinod and death
2) Confidence 0.56 Published 2002 Journal BMC Cancer Section Body Doc Link PMC130964 Disease Relevance 1.37 Pain Relevance 0.37
Previous studies have suggested that chemoprevention by non-steroidal anti-inflammatory drugs (NSAIDs) is blunted by the loss of a single component of the apoptotic machinery - the Bax protein.
Negative_regulation (loss) of Bax protein associated with inflammation, cinod and apoptosis
3) Confidence 0.43 Published 2006 Journal Anticancer Drugs Section Abstract Doc Link 16550006 Disease Relevance 1.35 Pain Relevance 0.24
P53 is known to regulate Bax expression, with inactivation of p53 leading to reduced Bax protein levels [69,70].
Negative_regulation (reduced) of Bax protein
4) Confidence 0.42 Published 2010 Journal World J Surg Oncol Section Body Doc Link PMC2913917 Disease Relevance 1.31 Pain Relevance 0
Cells from mice deficient for both Bax and Bak, but not cells deficient for one or the other only, are almost completely resistant to mitochondria-mediated apoptosis [37], suggesting that these proteins have redundant functions in this pathway.
Negative_regulation (deficient) of Bax associated with apoptosis
5) Confidence 0.41 Published 2002 Journal BMC Cancer Section Body Doc Link PMC130964 Disease Relevance 0.70 Pain Relevance 0.16
M resveratrol for 24 h resulted in the redistribution of Bax, regardless of p53-status, producing a distinctive, punctuate staining pattern in the cytosol with perinuclear concentration, resembling the pattern produced by the mitochondria-specific Mitotracker Red dye (Figure 2A).
Negative_regulation (redistribution) of Bax
6) Confidence 0.41 Published 2002 Journal BMC Cancer Section Body Doc Link PMC130964 Disease Relevance 0.12 Pain Relevance 0.04
After 4 degrees C storage and warm reperfusion, MEGX production was preserved in 24 h- and 48 h-stored bioreactors as well as a sharp increase of Bcl-2 and a decrease of Bax mRNAs.
Negative_regulation (decrease) of Bax associated with apoptosis
7) Confidence 0.40 Published 2003 Journal Int J Artif Organs Section Abstract Doc Link 12653348 Disease Relevance 0.57 Pain Relevance 0.07
In conclusion, we found that Bax/Bak-mediated MOMP is a key mechanism of diclofenac-induced lethal cell injury in human hepatocytes, and that CsA can prevent MOMP through inhibition of Bax activation.
Negative_regulation (inhibition) of Bax in hepatocytes associated with injury and diclofenac
8) Confidence 0.37 Published 2008 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 18191430 Disease Relevance 0.60 Pain Relevance 0.35
Nbk fails to induce apoptosis in the absence of Bax.
Negative_regulation (absence) of Bax associated with apoptosis
9) Confidence 0.35 Published 2005 Journal BMC Cancer Section Body Doc Link PMC1198222 Disease Relevance 0.64 Pain Relevance 0
The protein levels of Bcl-2 decreased and Bax increased in the mitochondrial fraction while the Bax protein decreased, and p53 and cytochrome c protein levels increased in the cytosolic fraction in HepG2 cells after capsaicin treatment for 24 h by Western blot.
Negative_regulation (decreased) of Bax associated with qutenza
10) Confidence 0.32 Published 2009 Journal Anticancer Res. Section Abstract Doc Link 19331147 Disease Relevance 0.31 Pain Relevance 0.88
Therefore any increase in bcl-2 or decrease in bax will push the balance towards chemo resistance and an increase in bax or decrease in bcl-2 will result in increased apoptosis [26-30].
Negative_regulation (decrease) of bax associated with apoptosis
11) Confidence 0.31 Published 2004 Journal BMC Cancer Section Body Doc Link PMC514705 Disease Relevance 1.38 Pain Relevance 0
This inhibition is associated with increased levels of the anti-apoptotic factors Bcl-xl and Bcl-2 as well as with decreased levels of Bax.
Negative_regulation (decreased) of Bax associated with apoptosis
12) Confidence 0.24 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2895614 Disease Relevance 1.31 Pain Relevance 0.27
In contrast, we find that TRAIL/Apo2L fails to activate caspase-9 or induce apoptosis in isogenic HCT116 colorectal cancer cells that are deficient in BAX, a proapoptotic gene that is mutated in >50% of colorectal cancers of the microsatellite mutator phenotype.
Negative_regulation (deficient) of BAX associated with colon cancer and apoptosis
13) Confidence 0.24 Published 2002 Journal Cancer Res. Section Abstract Doc Link 11912124 Disease Relevance 1.57 Pain Relevance 0.06
Loss of BAX also renders colorectal cancer cells resistant to TRAIL/Apo2L-mediated radiosensitization.
Negative_regulation (Loss) of BAX associated with colon cancer
14) Confidence 0.24 Published 2002 Journal Cancer Res. Section Abstract Doc Link 11912124 Disease Relevance 1.59 Pain Relevance 0.07
In context of its apoptosis-inducing properties, zinc has been shown to increase the expression of Bax, leading to a decrease in the Bcl-2/Bax ratio [101].
Negative_regulation (decrease) of Bax associated with apoptosis
15) Confidence 0.24 Published 2010 Journal International Journal of Environmental Research and Public Health Section Body Doc Link PMC2872358 Disease Relevance 1.41 Pain Relevance 0.04
This is not undisputed, because it has also been shown in another study that zinc can increase the expression of Bax, leading to an decreased Bcl-2/Bax ratio and the release of cytochrome-c from mitochondria [101].
Negative_regulation (decreased) of Bax
16) Confidence 0.24 Published 2010 Journal International Journal of Environmental Research and Public Health Section Body Doc Link PMC2872358 Disease Relevance 0.84 Pain Relevance 0
Recent studies have shown that pharmacological activation of these kinases is associated with recruitment of anti-apoptotic signaling components such as the phosphorylation and inhibition of the proapoptotic proteins Bax and Bad, the inhibition of caspase 3 activation, the phosphorylation and activation of p70S6K (which acts to inhibit Bad) and the phosphorylation and activation of the antiapoptotic protein Bcl-2 (Harada et al 2001; Hausenloy and Yellon 2007).
Negative_regulation (inhibition) of Bax associated with apoptosis
17) Confidence 0.18 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2291307 Disease Relevance 0.48 Pain Relevance 0.09
These results indicate that mitochondrial-mediated apoptosis in HepG2 cells, triggered by DLS, is predominantly associated with down-regulation of the Bcl-2/Bax expression ratio.Fig. 3Western blot analysis of the expression levels of caspase3, caspase9, Bcl-2, Bax, caspase8 and DR5 with the treatment of DLS for 24 h (All the experiments were repeated four times.)Fig. 4Bcl-2, Bax, DR5 protein expression in HepG2 cells (×200). a, c, e Immunocytochemistry of Bcl-2, Bax and DR5 staining in HepG2 cells for 24 h of treatment without DLS. b, d, f Immunocytochemistry of Bcl-2, Bax and DR5 staining in HepG2 cells for 24 h of treatment with 25 ?
Negative_regulation (regulation) of Bax associated with apoptosis
18) Confidence 0.18 Published 2009 Journal Mol Biol Rep Section Body Doc Link PMC2941086 Disease Relevance 0.64 Pain Relevance 0
Bcl-2 is the best described member of this family preventing Bax activation [51].
Negative_regulation (preventing) of Bax
19) Confidence 0.15 Published 2010 Journal International Journal of Cell Biology Section Body Doc Link PMC2841246 Disease Relevance 1.07 Pain Relevance 0
It has numerous proposed functions, including modulation of apoptosis by inhibition of Bax [59].
Negative_regulation (inhibition) of Bax associated with apoptosis
20) Confidence 0.15 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1906814 Disease Relevance 0.91 Pain Relevance 0.20

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