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Context Info
Confidence 0.60
First Reported 1998
Last Reported 2010
Negated 3
Speculated 0
Reported most in Abstract
Documents 13
Total Number 13
Disease Relevance 14.13
Pain Relevance 2.73

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

cytosol (BAK1) mitochondrion (BAK1) aging (BAK1)
endoplasmic reticulum (BAK1) intracellular (BAK1)
Anatomy Link Frequency
plasma 1
spinal cord 1
anterior 1
3T3-L1 1
reticulum 1
BAK1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Spinal cord 3 99.84 Very High Very High Very High
diclofenac 11 99.58 Very High Very High Very High
qutenza 11 99.48 Very High Very High Very High
cINOD 10 98.40 Very High Very High Very High
antagonist 7 85.12 High High
Thermal hyperalgesia 2 82.40 Quite High
Hyperalgesia 3 79.60 Quite High
Neuropathic pain 2 78.64 Quite High
Inflammation 34 76.80 Quite High
Glutamate 4 75.00 Quite High
Disease Link Frequency Relevance Heat
Apoptosis 331 100.00 Very High Very High Very High
Acute Renal Failure 83 99.72 Very High Very High Very High
Multiple Myeloma 4 99.68 Very High Very High Very High
Burns 74 99.50 Very High Very High Very High
Death 124 99.48 Very High Very High Very High
Injury 38 98.68 Very High Very High Very High
Toxicity 17 96.00 Very High Very High Very High
Parkinson's Disease 10 95.32 Very High Very High Very High
Endometrial Cancer 153 93.76 High High
Gliosis 1 92.44 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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 Bak associated with parkinson's disease and apoptosis
1) Confidence 0.60 Published 2005 Journal BMC Cancer Section Body Doc Link PMC1198222 Disease Relevance 0.71 Pain Relevance 0
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 Bak associated with diclofenac and death
2) Confidence 0.52 Published 2008 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 18191430 Disease Relevance 0.87 Pain Relevance 0.46
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 Bak associated with multiple myeloma and apoptosis
3) Confidence 0.51 Published 2007 Journal Apoptosis Section Abstract Doc Link 17136320 Disease Relevance 1.14 Pain Relevance 0
BAK-C is a new autostabilizing interbody cage which is implanted during an anterior cervical procedure to provide stability to the motion segment and allow fusion to occur.
Positive_regulation (implanted) of BAK in anterior
4) Confidence 0.49 Published 1998 Journal Acta Neurochir (Wien) Section Abstract Doc Link 9522900 Disease Relevance 0.18 Pain Relevance 0.06
Apoptosis induced by the mitochondrial pathway commences with Ca2+ release from the ER that leads to an increase of Ca2+ in the mitochondria as well as translocation of BAX into the mitochondria and BAK activation (23).
Positive_regulation (activation) of BAK associated with apoptosis
5) Confidence 0.45 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2585850 Disease Relevance 1.27 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 Bak associated with cinod and apoptosis
6) Confidence 0.43 Published 2006 Journal Anticancer Drugs Section Abstract Doc Link 16550006 Disease Relevance 1.36 Pain Relevance 0.26
The dual chemopreventive agent/death ligand treatments do not increase Fas, TNF receptor 1, Bak or c-myc expression (although salicylic acid moderately induces of Fas expression).
Neg (not) Positive_regulation (increase) of Bak associated with death
7) Confidence 0.38 Published 1999 Journal Biochim. Biophys. Acta Section Abstract Doc Link 9990295 Disease Relevance 0.94 Pain Relevance 0.23
Gene array analysis demonstrated that burns septic ARF group plasma induced an up-regulation of several pro-apoptotic genes such as Fas, Fas-Ligand (Fas-L), Bax and Bak and of positive regulators of apoptosis (Abl1, Gadd45a).
Positive_regulation (induced) of Bak in plasma associated with acute renal failure, burns and apoptosis
8) Confidence 0.24 Published 2008 Journal Crit Care Section Body Doc Link PMC2447585 Disease Relevance 1.59 Pain Relevance 0.07
Apoptosis was rapidly initiated after endoplasmic reticulum Ca2+ depletion, while the multidomain Bax/Bak proteins are strictly required for fast effector caspase activation and induction of intrinsic apoptosis.
Positive_regulation (required) of Bak in reticulum associated with apoptosis
9) Confidence 0.16 Published 2010 Journal International Journal of Molecular Sciences Section Body Doc Link PMC2852855 Disease Relevance 1.35 Pain Relevance 0.03
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.
Positive_regulation (activation) of Bak associated with apoptosis
10) Confidence 0.12 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1775042 Disease Relevance 0.38 Pain Relevance 0
The induction of apoptosis in 3T3-L1 preadipocytes by capsaicin was mediated through the activation of caspase-3, Bax, and Bak, and then through the cleavage of PARP and the down-regulation of Bcl-2.
Positive_regulation (activation) of Bak in 3T3-L1 associated with qutenza and apoptosis
11) Confidence 0.08 Published 2007 Journal J. Agric. Food Chem. Section Abstract Doc Link 17295509 Disease Relevance 0.85 Pain Relevance 0.83
Thus, loss of PTEN function leads to increased levels of phospho-AKT, activation of anti-apoptotic protein, and cell cycle progression [9].
Positive_regulation (activation) of anti-apoptotic protein associated with apoptosis
12) Confidence 0.01 Published 2010 Journal Obstetrics and Gynecology International Section Body Doc Link PMC2846683 Disease Relevance 1.79 Pain Relevance 0
An early (2-3 days post-CCI) E2F1- and p53-independent apoptosis appeared in the spinal cord as the pro-apoptotic bax gene increased (320 +/- 19%), followed by an increased expression of the anti-apoptotic bcl-2 and bcl-xL genes (60 +/- 11% and 110 +/- 15%, respectively) 7 days from CCI.
Positive_regulation (increased) of pro-apoptotic in spinal cord associated with injury, apoptosis and spinal cord
13) Confidence 0.00 Published 2004 Journal Neuropharmacology Section Abstract Doc Link 14975670 Disease Relevance 1.70 Pain Relevance 0.80

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