INT156016

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Context Info
Confidence 0.36
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 10
Total Number 10
Disease Relevance 7.42
Pain Relevance 2.64

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

cytosol (BCL2L1) mitochondrion (BCL2L1) growth (BCL2L1)
cytoskeleton (BCL2L1) nucleus (BCL2L1) intracellular (BCL2L1)
Anatomy Link Frequency
colon 2
neurons 1
BCL2L1 (Homo sapiens)
Pain Link Frequency Relevance Heat
cINOD 53 99.74 Very High Very High Very High
Inflammation 53 10.72 Low Low
cytokine 35 6.72 Low Low
COX-2 inhibitor 52 5.00 Very Low Very Low Very Low
Hippocampus 21 5.00 Very Low Very Low Very Low
Eae 18 5.00 Very Low Very Low Very Low
long-term potentiation 15 5.00 Very Low Very Low Very Low
Kinase C 15 5.00 Very Low Very Low Very Low
Neurotransmitter 15 5.00 Very Low Very Low Very Low
Central nervous system 12 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 643 100.00 Very High Very High Very High
Colon Cancer 38 99.80 Very High Very High Very High
Death 207 99.24 Very High Very High Very High
INFLAMMATION 70 97.40 Very High Very High Very High
Targeted Disruption 14 96.12 Very High Very High Very High
Papillomavirus Infection 1 95.52 Very High Very High Very High
Pancreatic Cancer 49 93.32 High High
Cancer 211 92.56 High High
Malignant Neoplastic Disease 5 92.16 High High
Lymphatic System Cancer 9 89.36 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
NSAIDs promote the dissociation of BAX and Bcl-X(L) and translocation of BAX to the mitochondria.
Bcl-X Binding (dissociation) of associated with cinod
1) Confidence 0.36 Published 2008 Journal Nutr Cancer Section Abstract Doc Link 19003586 Disease Relevance 1.21 Pain Relevance 0.91
These results suggest that NSAIDs induce apoptosis in colon cancer cells by dissociating BAX and Bcl-X(L), thereby promoting BAX mitochondrial translocation and multimerization.
Bcl-X Binding (dissociating) of in colon associated with colon cancer, cinod and apoptosis
2) Confidence 0.36 Published 2008 Journal Nutr Cancer Section Abstract Doc Link 19003586 Disease Relevance 1.19 Pain Relevance 0.82
NSAIDs downregulate Bcl-X(L) and dissociate BAX and Bcl-X(L) to induce apoptosis in colon cancer cells.
Bcl-X Binding (dissociate) of in colon associated with colon cancer, cinod and apoptosis
3) Confidence 0.36 Published 2008 Journal Nutr Cancer Section Title Doc Link 19003586 Disease Relevance 1.19 Pain Relevance 0.91
The interaction between Bcl-X–BAD (PDB 2BZW) was missed by our analysis because the ligand bound structure (2YXJ:N3C) was published too recently to be classified in the current SCOP domain database.
Bcl-X Binding (interaction) of
4) Confidence 0.36 Published 2010 Journal PLoS Computational Biology Section Body Doc Link PMC2816688 Disease Relevance 0.10 Pain Relevance 0
For instance, desphosphorylation of Bad allows it to interact with Bcl-xL and initiate cell death [43].
Bcl-xL Binding (interact) of associated with death
5) Confidence 0.26 Published 2005 Journal BMC Cancer Section Body Doc Link PMC1198222 Disease Relevance 0.90 Pain Relevance 0
Bax can form also a complex with the anti-apoptotic protein Bcl-xL [53] and Mcl-1 [14].
Bcl-xL Binding (complex) of associated with apoptosis
6) Confidence 0.10 Published 2010 Journal International Journal of Cell Biology Section Body Doc Link PMC2841246 Disease Relevance 1.09 Pain Relevance 0
Phosphorylation prevents Bad from binding either Bcl-2 or Bcl-XL and thus suppresses apoptosis.
Bcl-XL Binding (binding) of associated with apoptosis
7) Confidence 0.05 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2806309 Disease Relevance 0.81 Pain Relevance 0
In sympathetic neurons, following growth factor deprivation and failure of PI3K/Akt signaling, Bad is activated by dephosphorylation, dissociation from the molecular chaperone 14-3-3 and association with Bcl-XL.
Bcl-XL Binding (association) of in neurons
8) Confidence 0.04 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1775042 Disease Relevance 0.29 Pain Relevance 0
Bax and Bak activation is mediated by Bad, Bik, Bid, and Bim and is due to either the preferential interaction with Bcl-2 and Bcl-XL, or their release from these anti-apoptotic proteins, thus shifting the balance of the different heterodimers toward the formation of the proapoptotic Bax and Bak homodimers.
Bcl-XL Binding (interaction) of associated with apoptosis
9) Confidence 0.04 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1775042 Disease Relevance 0.37 Pain Relevance 0
In viable cells, Bcl-XL binds Bax and Bak, thus keeping them in an inactive form.
Bcl-XL Binding (binds) of
10) Confidence 0.03 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1775042 Disease Relevance 0.28 Pain Relevance 0

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