INT135441

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Context Info
Confidence 0.67
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 15
Total Number 15
Disease Relevance 6.60
Pain Relevance 7.87

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

mitochondrion (Map2k1) Golgi apparatus (Map2k1) cytoplasm (Map2k1)
cell proliferation (Map2k1) cytosol (Map2k1) mitosis (Map2k1)
Anatomy Link Frequency
brain stem 5
cardiomyocyte 1
brain 1
cortex 1
Map2k1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Rostral ventrolateral medulla 440 99.84 Very High Very High Very High
agonist 8 99.46 Very High Very High Very High
opioid receptor 2 99.30 Very High Very High Very High
Kappa opioid receptor 6 99.08 Very High Very High Very High
Kinase C 42 98.72 Very High Very High Very High
Morphine 30 98.64 Very High Very High Very High
Pain 60 97.92 Very High Very High Very High
medulla 91 97.88 Very High Very High Very High
Opioid 12 95.72 Very High Very High Very High
withdrawal 11 95.44 Very High Very High Very High
Disease Link Frequency Relevance Heat
Death 503 99.56 Very High Very High Very High
Stress 23 98.88 Very High Very High Very High
Pain 82 97.92 Very High Very High Very High
Opiate Addiction 10 95.72 Very High Very High Very High
Pressure Volume 2 Under Development 35 92.92 High High
Poisoning 56 86.84 High High
Chondrocalcinosis 12 86.72 High High
Bacillus Anthracis Infection 28 86.32 High High
Nociception 14 84.08 Quite High
Recurrence 2 81.60 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Stimulation of mitogen-activated protein kinase kinases (MEK1/2) by mu-, delta- and kappa-opioid receptor agonists in the rat brain: regulation by chronic morphine and opioid withdrawal.
Positive_regulation (Stimulation) of MEK1 in brain associated with agonist, kappa opioid receptor, withdrawal, opioid and morphine
1) Confidence 0.67 Published 2006 Journal Eur. J. Pharmacol. Section Title Doc Link 16678156 Disease Relevance 0.27 Pain Relevance 1.09
Similarly, the selective delta-opioid receptor agonist SNC-80 (10 mg/kg, 30 min) increased MEK1/2 activity in the cortex (60%) that was antagonized by naltrindole.
Positive_regulation (increased) of MEK1 in cortex associated with agonist and opioid receptor
2) Confidence 0.49 Published 2006 Journal Eur. J. Pharmacol. Section Abstract Doc Link 16678156 Disease Relevance 0.27 Pain Relevance 1.38
Furthermore, although our in vitro data do not favor a major role of stress signaling MEK1/2, p38 MAP kinase, JNK and ERK in lethal toxin-elicited cardiomyocyte response in vitro, the fact that these stress signaling molecules were significantly down-regulated (MEK1/2, p38 MAP kinase and ERK) or upregulated (JNK) in the in vivo setting of lethal toxin exposure suggest a time-dependent response for stress signaling activation.
Positive_regulation (upregulated) of MEK1 in cardiomyocyte associated with stress
3) Confidence 0.45 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954163 Disease Relevance 0.59 Pain Relevance 0.04
Furthermore, as the mitogen-activated protein kinase kinase 1 (MAPKK1) was increased significantly in the stages of establishment and reinstatement, we confirmed the change of activated extracellular signal-regulated kinase (ERK) by Western blotting in VTA tissue and cultured cell.
Positive_regulation (increased) of MAPKK1 associated with ventral tegmentum
4) Confidence 0.37 Published 2010 Journal J. Neurosci. Res. Section Abstract Doc Link 20091775 Disease Relevance 0.14 Pain Relevance 1.09
Furthermore, as the mitogen-activated protein kinase kinase 1 (MAPKK1) was increased significantly in the stages of establishment and reinstatement, we confirmed the change of activated extracellular signal-regulated kinase (ERK) by Western blotting in VTA tissue and cultured cell.
Positive_regulation (increased) of mitogen-activated protein kinase kinase 1 associated with ventral tegmentum
5) Confidence 0.37 Published 2010 Journal J. Neurosci. Res. Section Abstract Doc Link 20091775 Disease Relevance 0.15 Pain Relevance 1.10
We suggest, to some extent, that it maybe due to the differential activation and regulation of upstream activators for ERK1 and ERK2 (MEK1 or MEK2, for example) in different areas under the pain states.
Positive_regulation (activators) of MEK1 associated with pain
6) Confidence 0.24 Published 2007 Journal BMC Neurosci Section Body Doc Link PMC1949833 Disease Relevance 0.47 Pain Relevance 0.73
Pharmacological blockade was again used to ascertain that these temporally correlated biochemical changes are causally linked to MEK1/2 or ERK1/2 activation in RVLM during experimental brain stem death.
Positive_regulation (activation) of MEK1 in brain stem associated with rostral ventrolateral medulla and death
7) Confidence 0.20 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2848001 Disease Relevance 0.60 Pain Relevance 0.32
Activation of MEK1/2, ERK1/2 or MNK1/2 in RVLM sustains central cardiovascular regulation associated with experimental brain stem death
Positive_regulation (Activation) of MEK1 in brain stem associated with rostral ventrolateral medulla and death
8) Confidence 0.20 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2848001 Disease Relevance 0.62 Pain Relevance 0.37
Our results demonstrated that activation of MEK1/2, ERK1/2 and MNK1/2 in RVLM plays a preferential pro-life role by sustaining central cardiovascular regulatory functions during brain stem death via upregulation of the NOS I/PKG signaling cascade in RVLM.


Positive_regulation (activation) of MEK1 in brain stem associated with rostral ventrolateral medulla and death
9) Confidence 0.14 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2848001 Disease Relevance 0.46 Pain Relevance 0.17
Based on a clinically relevant experimental model [4], the present study provided novel demonstrations that MEK1/2 or ERK1/2 activation in RVLM sustains central cardiovascular regulation during the progression towards brain stem death.
Positive_regulation (activation) of MEK1 in brain stem associated with rostral ventrolateral medulla and death
10) Confidence 0.14 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2848001 Disease Relevance 0.49 Pain Relevance 0.33
Activation of MEK1/2 or ERK1/2 is not responsible for the augmentation of NOS II or peroxynitrite in RVLM during the pro-death phase
Positive_regulation (Activation) of MEK1 associated with rostral ventrolateral medulla and death
11) Confidence 0.14 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2848001 Disease Relevance 0.55 Pain Relevance 0.37
Activation of MEK1/2 or ERK1/2 underlies the augmentation of NOS I or PKG in RVLM during the pro-life phase
Positive_regulation (Activation) of MEK1 associated with rostral ventrolateral medulla
12) Confidence 0.14 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2848001 Disease Relevance 0.41 Pain Relevance 0.22
Our results demonstrated that activation of MEK1/2, ERK1/2 and MNK1/2 in RVLM plays a preferential pro-life role by sustaining the central cardiovascular regulatory machinery during brain stem death via upregulation of NOS I/PKG signaling cascade in RVLM.



Positive_regulation (activation) of MEK1 in brain stem associated with rostral ventrolateral medulla and death
13) Confidence 0.14 Published 2010 Journal J Biomed Sci Section Abstract Doc Link PMC2848001 Disease Relevance 0.57 Pain Relevance 0.20
As such, MEK1/2 or ERK1/2 activation in RVLM may also lead to an antagonism of this augmentation.
Positive_regulation (activation) of MEK1 associated with rostral ventrolateral medulla
14) Confidence 0.14 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2848001 Disease Relevance 0.47 Pain Relevance 0.37
Induction of Ank is mediated by the dual activation of Ras, Raf-1, and MEK-1/ERK cascade and Ca2+-dependent PKC but is independent of the Smad signaling pathway.
Positive_regulation (activation) of MEK-1 associated with kinase c
15) Confidence 0.06 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2246241 Disease Relevance 0.53 Pain Relevance 0.09

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