INT112692

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Context Info
Confidence 0.80
First Reported 2003
Last Reported 2010
Negated 3
Speculated 0
Reported most in Body
Documents 31
Total Number 33
Disease Relevance 20.97
Pain Relevance 3.98

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
livers 1
spinal cords 1
colon 1
proximal 1
apoptotic cell 1
Bax (Mus musculus)
Pain Link Frequency Relevance Heat
Paracetamol 47 99.72 Very High Very High Very High
cytokine 71 97.12 Very High Very High Very High
rheumatoid arthritis 114 93.52 High High
Dismenorea 1 89.92 High High
addiction 29 88.96 High High
cINOD 10 83.84 Quite High
Nerve growth factor 3 80.96 Quite High
Osteoarthritis 6 76.64 Quite High
Inflammatory response 49 73.92 Quite High
Inflammation 245 64.24 Quite High
Disease Link Frequency Relevance Heat
Apoptosis 944 100.00 Very High Very High Very High
Parkinson's Disease 375 99.96 Very High Very High Very High
Overdose 9 99.82 Very High Very High Very High
Death 417 99.24 Very High Very High Very High
Cv Unclassified Under Development 205 99.04 Very High Very High Very High
Hepatotoxicity 17 99.04 Very High Very High Very High
Necrosis 45 98.40 Very High Very High Very High
Colon Cancer 31 97.88 Very High Very High Very High
Stress 156 94.96 High High
Rheumatoid Arthritis 116 93.52 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Because mitochondrial translocation of Bax can initiate these events, we investigated the potential role of Bax in the pathophysiology of hepatic necrosis after 300 mg/kg APAP in fasted C57BL/6 mice.
Localization (translocation) of Bax associated with necrosis and paracetamol
1) Confidence 0.80 Published 2008 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 17906064 Disease Relevance 0.53 Pain Relevance 0.53
We concluded that the rapid mitochondrial Bax translocation after APAP overdose has no effect on peroxynitrite formation but that it contributes to the mitochondrial release of proteins, which cause nuclear DNA fragmentation.
Localization (translocation) of Bax associated with paracetamol and overdose
2) Confidence 0.80 Published 2008 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 17906064 Disease Relevance 0.69 Pain Relevance 0.43
APAP overdose induced Bax translocation from the cytosol to the mitochondria as early as 1 h after APAP injection.
Localization (translocation) of Bax associated with paracetamol and overdose
3) Confidence 0.80 Published 2008 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 17906064 Disease Relevance 0.57 Pain Relevance 0.60
DIM-C-pPhOCH(3) induced caspase-dependent apoptosis in RKO colon cancer cells through decreased mitochondrial membrane potential which is accompanied by increased mitochondrial bax/bcl-2 ratios and release of cytochrome c into the cytosol.
Localization (release) of bax in colon associated with colon cancer and apoptosis
4) Confidence 0.73 Published 2008 Journal Mol. Carcinog. Section Abstract Doc Link 17957723 Disease Relevance 0.70 Pain Relevance 0.12
Mitochondrial bax translocation accelerates DNA fragmentation and cell necrosis in a murine model of acetaminophen hepatotoxicity.
Localization (translocation) of bax associated with necrosis, paracetamol and hepatotoxicity
5) Confidence 0.70 Published 2008 Journal J. Pharmacol. Exp. Ther. Section Title Doc Link 17906064 Disease Relevance 0.58 Pain Relevance 0.58
We investigated if BAX aggregation was altered at non-lethal levels of fusion protein by monitoring the subcellular localization of GFP-BAX in HCT116BAX-/- cells, before and after, indomethacin treatment (Figure 4).
Localization (localization) of GFP-BAX
6) Confidence 0.70 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2964639 Disease Relevance 0.39 Pain Relevance 0
Others, using similar GFP-BAX constructs, had demonstrated that BAX localization changed from a diffuse labeling pattern to more punctate foci, co-localizing with mitochondrial markers, as active protein translocates and aggregates to the MOM [22,23].
Localization (localization) of BAX
7) Confidence 0.70 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2964639 Disease Relevance 0.27 Pain Relevance 0
One potential target of JNK is Bax translocation, which was enhanced by APAP and blocked by the JNK inhibitor.
Localization (translocation) of Bax
8) Confidence 0.68 Published 2006 Journal Gastroenterology Section Body Doc Link 16831600 Disease Relevance 0.12 Pain Relevance 0
In this model, the expression of BH3-only proteins competed with BCLXL:BAX dimers and facilitated the release of BAX allowing to become active.
Localization (release) of BAX
9) Confidence 0.61 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2964639 Disease Relevance 0.74 Pain Relevance 0.08
The impairment of BAX translocation and/or aggregation in cells expressing sub-lethal levels can be interpreted in several ways, depending on the rate-limiting step for BAX activation.
Localization (translocation) of BAX
10) Confidence 0.61 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2964639 Disease Relevance 0.63 Pain Relevance 0.04
Current models suggest that very few cytosolic BAX molecules actually need to be independently activated (by BH3-only proteins) and translocated, since once they are present in the MOM they act as a sink to capture other BAX molecules, even if the latter are missing their C-terminal mitochondrial targeting domains [4,31].
Localization (translocated) of BAX
11) Confidence 0.61 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2964639 Disease Relevance 0.26 Pain Relevance 0.03
At the same time, tBid became detectable in the mitochondrial fraction, and concomitantly, Bax was found translocated to mitochondria.
Localization (translocated) of Bax
12) Confidence 0.59 Published 2003 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 12946648 Disease Relevance 0.44 Pain Relevance 0.57
During apoptosis, translocation of Bax from the cytosol to the mitochondria in the spinal cords of G93A mice [88] triggers the release of cytochrome c from the mitochondria [89].
Localization (translocation) of Bax in spinal cords associated with apoptosis
13) Confidence 0.49 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2827549 Disease Relevance 0.84 Pain Relevance 0.03
Immunohistochemical localization of nitrotyrosine, PARP, ICAM-1, P-Selectin, Bax, Bcl-2, TNF-?
Localization (localization) of Bax
14) Confidence 0.48 Published 2010 Journal J Inflamm (Lond) Section Body Doc Link PMC2844385 Disease Relevance 0 Pain Relevance 0.03
It is notable that BAX, which helps mediate Caspase-3 inducible apoptosis, is a common target of MMR mutations.
Localization (target) of BAX associated with apoptosis
15) Confidence 0.45 Published 2006 Journal Nucleic Acids Research Section Body Doc Link PMC1361617 Disease Relevance 1.01 Pain Relevance 0
Bax did not translocate to mitochondria and Bax antisense oligodeoxynucleotides were not protective.
Neg (not) Localization (translocate) of Bax
16) Confidence 0.39 Published 2005 Journal Kidney Int. Section Body Doc Link 15673306 Disease Relevance 0.06 Pain Relevance 0
In addition to the release of cytochrome c, BAX-dependent mitochondrial dysfunction also disrupts electron transport thereby destabilizing the proton gradient across the inner membrane, causing a loss of ATP production and the formation of superoxide anions and other free radicals.
Localization (release) of BAX-dependent associated with parkinson's disease
17) Confidence 0.35 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2964639 Disease Relevance 0.61 Pain Relevance 0
Furthermore, the downregulation of NP-1 transcripts by short interfering RNA caused spontaneous synoviocyte apoptosis, which was associated with both a decrease in Bcl-2 expression and an increase in Bax translocation to mitochondria.
Localization (translocation) of Bax associated with apoptosis
18) Confidence 0.29 Published 2008 Journal Mediators of Inflammation Section Body Doc Link PMC2638142 Disease Relevance 0.85 Pain Relevance 0.33
Furthermore, VEGF165 completely blocked SNP-induced Bcl-2 downregulation and SNP-induced Bax translocation from the cytosol to mitochondria.
Localization (translocation) of Bax
19) Confidence 0.29 Published 2008 Journal Mediators of Inflammation Section Body Doc Link PMC2638142 Disease Relevance 0.91 Pain Relevance 0.26
However, by inhibiting Bcl-2 proteins, ApoG2 still helped release pro-apoptotic proteins, such as Bax and Bak, and irreversibly damaged mitochondria and induced cell apoptotic [5].
Localization (release) of Bax associated with apoptosis
20) Confidence 0.24 Published 2009 Journal J Transl Med Section Body Doc Link PMC2742515 Disease Relevance 1.14 Pain Relevance 0.09

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