INT154970

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Context Info
Confidence 0.74
First Reported 2006
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 15
Total Number 15
Disease Relevance 11.12
Pain Relevance 2.11

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
spinal cord 1
pores 1
brain 1
heart 1
Bax (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Hippocampus 6 98.64 Very High Very High Very High
anesthesia 12 98.00 Very High Very High Very High
Spinal cord 4 97.44 Very High Very High Very High
Pain 13 96.00 Very High Very High Very High
ischemia 202 91.88 High High
Immobilon 1 87.48 High High
IPN 1 85.04 High High
diclofenac 5 81.68 Quite High
Inflammation 85 75.48 Quite High
Lasting pain 1 73.16 Quite High
Disease Link Frequency Relevance Heat
Apoptosis 532 99.56 Very High Very High Very High
Stress 46 98.52 Very High Very High Very High
Cancer 49 98.50 Very High Very High Very High
Overdose 5 97.44 Very High Very High Very High
Pain 12 96.00 Very High Very High Very High
Myocardial Infarction 29 95.84 Very High Very High Very High
Hypoxia 119 95.08 Very High Very High Very High
Injury 117 94.40 High High
Death 100 94.24 High High
Cv Unclassified Under Development 133 91.88 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Nimesulide exposure increased intracellular ROS, translocation of Bax and Bcl2 followed by mitochondrial depolarization and cytochrome c (Cyt c) release along with caspase-9/-3 activity confirming involvement of mitochondria in nimesulide induced apoptosis.
Localization (translocation) of Bax associated with apoptosis
1) Confidence 0.74 Published 2010 Journal Toxicol In Vitro Section Abstract Doc Link 19772912 Disease Relevance 0.74 Pain Relevance 0.07
These results showed an increased ratio of Bax/Bcl-2 and activated caspase-3 in hippocampus and dorsal lumbar spinal cord of animals treated with pain and IMO stress; these effects were reduced in ADX animals.
Localization (ratio) of Bax in spinal cord associated with stress, pain, hippocampus and spinal cord
2) Confidence 0.74 Published 2008 Journal Neuroscience Section Abstract Doc Link 18822355 Disease Relevance 1.75 Pain Relevance 1.05
Andrographolide induces apoptosis in human cancer cells via the activation of caspase 8, pro-apoptotic Bcl-2 family members Bax conformational change, release of cytochrome C from mitochondria and activation of caspase cascade [52] and/or via the activation of tumour suppressor p53 by ROS-dependent c-Jun NH2-terminal kinase (JNK) activation, thereby increasing p53 phosphorylation and protein stabilization [53,54].
Localization (release) of Bax associated with cancer and apoptosis
3) Confidence 0.73 Published 2010 Journal Chin Med Section Body Doc Link PMC2881933 Disease Relevance 1.13 Pain Relevance 0
DMH treatment reduced the mitochondrial translocation of Bax whereas cytochrome c was found to be located prominently in the mitochondria.
Localization (translocation) of Bax
4) Confidence 0.67 Published 2010 Journal Oncol. Res. Section Abstract Doc Link 20681407 Disease Relevance 0.39 Pain Relevance 0.27
When stimulated, Bax is activated and translocated to the mitochondria, where it forms pores in the outer membrane by binding with the adenine nucleotide translocator leading to permeabilization of the mitochondria [11-13].
Localization (translocated) of Bax in pores
5) Confidence 0.66 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2765238 Disease Relevance 0.76 Pain Relevance 0.10
In the present study, TUNEL positivity and the immunohistochemical localization of Bax, an inducer of apoptosis and Bcl-2 proteins, inhibitors of apoptosis were studied to delineate the involvement of apoptosis in I-R induced injury.
Localization (localization) of Bax associated with injury and apoptosis
6) Confidence 0.47 Published 2006 Journal BMC Complement Altern Med Section Body Doc Link PMC1397864 Disease Relevance 1.72 Pain Relevance 0.05
Briefly, 4–6 micron thick fixed paraffin tissue sections were subjected to the following immunohistochemical procedure for the localization of Bax and Bcl-2 proteins using specific mouse monoclonal primary antibodies.
Localization (localization) of Bax
7) Confidence 0.47 Published 2006 Journal BMC Complement Altern Med Section Body Doc Link PMC1397864 Disease Relevance 0.46 Pain Relevance 0.14
The relative involvement of apoptosis in cardiac I-R was evaluated and the anti-apoptotic activity of these herbs was investigated using immunohistochemical localization of Bax and Bcl-2 proteins and TUNEL staining.
Localization (localization) of Bax associated with apoptosis
8) Confidence 0.47 Published 2006 Journal BMC Complement Altern Med Section Body Doc Link PMC1397864 Disease Relevance 0.75 Pain Relevance 0.03
i) Immunostaining for the localization of Bax and Bcl-2 proteins
Localization (localization) of Bax
9) Confidence 0.47 Published 2006 Journal BMC Complement Altern Med Section Body Doc Link PMC1397864 Disease Relevance 0.53 Pain Relevance 0.18
The following primary antibodies were used: rabbit anti-ERK, mouse anti-phospho ERK, mouse anti-Bcl-2, rabbit anti-Bax (Assay Designs, Ann Arbor, MI, USA), mouse anti-SERCA2a, mouse anti-NCX (Affinity Bioreagents, Rockford, IL, USA), and mouse anti-?
Localization (used) of Bax
10) Confidence 0.29 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2824862 Disease Relevance 0.12 Pain Relevance 0
In addition, activaton of Erk 1/2 inhibits the conformational change in Bax protein and cytochrome c-induced caspase activation, thereby preventing apoptosis.31 The anti-apoptotic protein Bcl-2 was identified in the outer mitochondrial membrane and attenuates cellular injury by inhibiting cytochrome c translocation, preventing injurious Ca2+ release from the endoplasmic reticulum32 and inhibiting Bax translocation from the cytoplasm to the mitochondria.33 During IPC, an increase in Bcl-2 concomitant with a decrease in the proapoptotic protein Bax was observed in the isolated rat heart.34 It has been reported that overexpression of Bax can affect the storage of Ca2+ in the intracellular membranes, and changes in intracellular Ca2+ storage can feed back to the translocation of Bax from cytosol to intracellular membranes.35 Our results demonstrated that the thiopental-induced protective effect against hypoxia-reoxygenation injury was associated with an increase in Bcl-2 expression, decrease in Bax, and attenuation of mitochondrial cytochrome c release, resulting in the reduction of caspase-3 activity.
Localization (translocation) of Bax in heart associated with hypoxia, injury and apoptosis
11) Confidence 0.27 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2824862 Disease Relevance 0.69 Pain Relevance 0
Bax is translocated to mitochondria where it releases cytochrome c into the cytosol to interact with Apaf-1 to activate caspase-9, which in turn activates downstream caspases, such as active caspase-3 [26].
Localization (translocated) of Bax
12) Confidence 0.22 Published 2011 Journal Evidence-based Complementary and Alternative Medicine : eCAM Section Body Doc Link PMC2975073 Disease Relevance 1.07 Pain Relevance 0.10
After blockade of non-specific binding sites, membranes were incubated for 2 h at room temperature with a mouse monoclonal anti-Bcl-xL (1:1,000; BD PharMingen, Heidelberg, Germany) or a mouse monoclonal anti-Bax antibody (1:250; BD PharMingen), followed by a secondary peroxidase-linked anti-mouse antibody (BcL-xL 1:10,000 and Bax 1:20,000; Sigma).
Localization (secondary) of Bax
13) Confidence 0.15 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2592699 Disease Relevance 0 Pain Relevance 0.04
B)- and p53-dependent pathways, decreased Bcl-2 to Bax ratio, release of cytochrome c oxidase from mitochondria and caspase activation, and eventually activate DNA-breaking enzymes and the energy-consuming DNA repair enzymes resulting in DNA breakdown and cell death.5,6 Massive cell death in the brain harms neural network and ultimately impairs neurological functions.
Localization (release) of Bax in brain associated with death
14) Confidence 0.13 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2695239 Disease Relevance 0.55 Pain Relevance 0.07
Mechanistic events of how Mito-KATP exerts its protective effect has been unclear, but a recent study showed that activation of Mito-KATP by diazoxide increases the association of Bcl-2 with mitochondria, while prevents Bax translocation to mitochondria [74].


Localization (translocation) of Bax
15) Confidence 0.10 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2647147 Disease Relevance 0.46 Pain Relevance 0

General Comments

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