INT73595

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Context Info
Confidence 0.61
First Reported 1998
Last Reported 2010
Negated 4
Speculated 1
Reported most in Body
Documents 61
Total Number 62
Disease Relevance 56.97
Pain Relevance 7.82

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
MCF-7 3
cleavage 2
plasma 1
hepatocytes 1
pore 1
BAX (Homo sapiens)
Pain Link Frequency Relevance Heat
aspirin 39 99.60 Very High Very High Very High
diclofenac 35 99.58 Very High Very High Very High
Morphine 17 99.00 Very High Very High Very High
cINOD 105 98.94 Very High Very High Very High
palliative 5 98.60 Very High Very High Very High
Dismenorea 2 98.52 Very High Very High Very High
Inflammation 272 98.32 Very High Very High Very High
dexamethasone 254 98.32 Very High Very High Very High
Kinase C 24 97.52 Very High Very High Very High
Inflammatory marker 2 95.64 Very High Very High Very High
Disease Link Frequency Relevance Heat
Apoptosis 2328 100.00 Very High Very High Very High
Stress 152 99.96 Very High Very High Very High
Acute Renal Failure 83 99.72 Very High Very High Very High
Multiple Myeloma 42 99.68 Very High Very High Very High
Stomach Cancer 23 99.64 Very High Very High Very High
Death 464 99.62 Very High Very High Very High
Burns 74 99.50 Very High Very High Very High
Breast Cancer 170 99.32 Very High Very High Very High
Cancer 1213 99.14 Very High Very High Very High
INFLAMMATION 336 98.82 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Diclofenac induced early (9 h) activation of Bax and Bak and caused mitochondrial translocation of Bax, indicating that MOMP was involved in cell death.
Positive_regulation (activation) of Bax associated with diclofenac and death
1) Confidence 0.61 Published 2008 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 18191430 Disease Relevance 0.87 Pain Relevance 0.46
Diclofenac also induced early Bid activation (tBid formation, 6 h), which is an upstream mechanism that initiates Bax activation and mitochondrial translocation.
Positive_regulation (activation) of Bax associated with diclofenac
2) Confidence 0.61 Published 2008 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 18191430 Disease Relevance 0.76 Pain Relevance 0.39
BH3 peptides from Bad and Bik cannot directly activate Bax or Bak, but instead bind anti-apoptotic members of BCL-2, resulting in displacement of Bid-like BH3 domains which initiate mitochondrial dysfunction.
Neg (cannot) Positive_regulation (activate) of Bax associated with parkinson's disease and apoptosis
3) Confidence 0.57 Published 2005 Journal BMC Cancer Section Body Doc Link PMC1198222 Disease Relevance 0.70 Pain Relevance 0
Here, we have shown that amygdalin induces apoptotic cell death in human DU145 and LNCaP prostate cancer cells by caspase-3 activation through down-regulation of Bcl-2 and up-regulation of Bax.
Positive_regulation (up-regulation) of Bax in apoptotic cell associated with prostate cancer, apoptosis and death
4) Confidence 0.56 Published 2006 Journal Biol. Pharm. Bull. Section Abstract Doc Link 16880611 Disease Relevance 1.54 Pain Relevance 0.06
Differential upregulation of the apoptotic mediators p53, Bax, cytochrome c, and caspase-3 and -9, and downregulation of antiapoptotic Bcl-2, was observed in CP.
Positive_regulation (upregulation) of Bax
5) Confidence 0.53 Published 2008 Journal J. Gastroenterol. Section Body Doc Link 18600392 Disease Relevance 0.07 Pain Relevance 0
Thus, in contrast to NSAIDs, RS may remain effective as a pro-apoptotic chemopreventive as long as Bax and Bak have not both been inactivated during clonal selection.
Neg (not) Positive_regulation (inactivated) of Bax associated with cinod and apoptosis
6) Confidence 0.50 Published 2006 Journal Anticancer Drugs Section Abstract Doc Link 16550006 Disease Relevance 1.37 Pain Relevance 0.26
We have shown that RNA levels of proapoptotic bax were consistently decreased after marathon, whereas, RNA levels of antiapoptotic bcl-2 were slightly increased after marathon thereby causing a decreased bax: bcl-2 ratio (Figure 2B, C).
Positive_regulation (causing) of bax
7) Confidence 0.49 Published 2010 Journal BMC Physiol Section Body Doc Link PMC2893521 Disease Relevance 0.58 Pain Relevance 0
Thus, we calculated bax: bcl-2 ratio in the same group before and after marathon and such ratio was attenuated after marathon (Figure 2B, C).


Positive_regulation (calculated) of bax
8) Confidence 0.49 Published 2010 Journal BMC Physiol Section Body Doc Link PMC2893521 Disease Relevance 0.14 Pain Relevance 0
After an apoptotic stimulus, Bax is translocated into the mitochondria and promotes the release of cytochrome c [28], possibly by forming a pore [29] or a voltage-dependent anion channel in the outer mitochondrial membrane.
Spec (possibly) Positive_regulation (promotes) of Bax in pore associated with apoptosis
9) Confidence 0.49 Published 2009 Journal Journal of Oncology Section Body Doc Link PMC2730474 Disease Relevance 0.95 Pain Relevance 0
We have shown that RNA levels of proapoptotic bax were consistently decreased after marathon, whereas, RNA levels of antiapoptotic bcl-2 were slightly increased after marathon thereby causing a decreased bax: bcl-2 ratio (Figure 2B, C).
Positive_regulation (decreased) of bax
10) Confidence 0.49 Published 2010 Journal BMC Physiol Section Body Doc Link PMC2893521 Disease Relevance 0.57 Pain Relevance 0
In other sporadic forms of PD, additional biochemical abnormalities such as nuclear translocation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (Tatton et al 2003) and activation of proapoptotic proteins (eg, bax, caspases) (Hartmann et al 2000; Tatton 2000) have been identified.
Positive_regulation (activation) of bax associated with congenital anomalies and disease
11) Confidence 0.49 Published 2007 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2386362 Disease Relevance 1.37 Pain Relevance 0.06
TMZ induced apoptosis with an increase in Bax:Bcl-2 ratio
Positive_regulation (increase) of Bax associated with apoptosis
12) Confidence 0.48 Published 2004 Journal Mol Cancer Section Body Doc Link PMC544397 Disease Relevance 0.57 Pain Relevance 0.23
Moreover, the inhibition of apoptosis was correlated with an increase in bcl-2/bax ratio.
Positive_regulation (increase) of bax associated with apoptosis
13) Confidence 0.45 Published 2002 Journal Int. J. Oncol. Section Abstract Doc Link 12012007 Disease Relevance 0.71 Pain Relevance 0.13
We observed that IR-induced bax and p21(WAF1/Cip1) protein expression were attenuated selectively in normal stromal and epithelial cell cultures, yet maintained their p53-dependency in malignant cell lines.
Positive_regulation (induced) of bax in epithelial cell associated with malignant neoplastic disease
14) Confidence 0.45 Published 2003 Journal Prostate Cancer Prostatic Dis. Section Abstract Doc Link 12664070 Disease Relevance 0.90 Pain Relevance 0.10
Oridonin activated the caspase 3–dependent apoptotic pathway through up-regulation of Bax and down-regulation of Bcl-2, which promotes release of cytochrome c (Chen et al. 2005; Liu et al. 2006).
Positive_regulation (up-regulation) of Bax associated with apoptosis
15) Confidence 0.45 Published 2008 Journal Environ Health Perspect Section Body Doc Link PMC2535615 Disease Relevance 1.37 Pain Relevance 0
Our results demonstrate a novel mechanism of sulindac-induced apoptosis in human MM cells, namely, accumulation of p53, Bax, and Bak in mitochondria mediated by p38 MAPK activation downstream of ROS production.
Positive_regulation (accumulation) of Bax associated with multiple myeloma and apoptosis
16) Confidence 0.45 Published 2007 Journal Apoptosis Section Abstract Doc Link 17136320 Disease Relevance 1.14 Pain Relevance 0
The siRNA for PUMA inhibited the celecoxib-induced activation and translocation of Bax, release of cytochrome c into the cytosol and induction of apoptosis, suggesting that PUMA plays an important role in celecoxib-induced mitochondrial dysfunction and the resulting apoptosis.
Positive_regulation (activation) of Bax associated with parkinson's disease and apoptosis
17) Confidence 0.45 Published 2007 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 17368424 Disease Relevance 1.01 Pain Relevance 0.20
Furthermore, when cultures were treated with resveratrol and were separated into cell fractions after 24 h, Bax protein accumulated in the high membrane fractions enriched for mitochondria, again regardless of p53-status (Figure 2C).
Positive_regulation (accumulated) of Bax protein
18) Confidence 0.44 Published 2002 Journal BMC Cancer Section Body Doc Link PMC130964 Disease Relevance 0.29 Pain Relevance 0.04
Resveratrol at physiological doses can induce a Bax-mediated and a Bax-independent mitochondrial apoptosis.
Positive_regulation (induce) of Bax-independent associated with apoptosis
19) Confidence 0.44 Published 2002 Journal BMC Cancer Section Abstract Doc Link PMC130964 Disease Relevance 1.03 Pain Relevance 0
We have recently reported that the polyphenol resveratrol present in some foods can increase the steady-state levels of pro-apoptotic Bax protein and induce a mitochondria-mediated apoptosis in HCT116 cells independently of p53 [14].
Positive_regulation (increase) of Bax protein associated with apoptosis
20) Confidence 0.44 Published 2002 Journal BMC Cancer Section Body Doc Link PMC130964 Disease Relevance 0.94 Pain Relevance 0

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