INT158416

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Context Info
Confidence 0.67
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 19
Total Number 19
Disease Relevance 5.32
Pain Relevance 4.18

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

nucleoplasm (Mapk1) mitochondrion (Mapk1) protein complex (Mapk1)
cytoplasm (Mapk1) cytosol (Mapk1) signal transduction (Mapk1)
Anatomy Link Frequency
band 2
neuronal 1
stromal cells 1
spinal cord 1
nucleus 1
Mapk1 (Mus musculus)
Pain Link Frequency Relevance Heat
c fibre 3 99.44 Very High Very High Very High
Spinal cord 50 99.28 Very High Very High Very High
Dorsal horn 10 98.94 Very High Very High Very High
antagonist 138 98.52 Very High Very High Very High
Hippocampus 12 98.44 Very High Very High Very High
long-term potentiation 104 97.64 Very High Very High Very High
Neuropathic pain 68 95.12 Very High Very High Very High
tetrodotoxin 2 94.32 High High
agonist 56 91.28 High High
Traumatic nerve injury 3 90.12 High High
Disease Link Frequency Relevance Heat
Apoptosis 70 99.20 Very High Very High Very High
Disease 22 98.58 Very High Very High Very High
Nervous System Injury 27 98.36 Very High Very High Very High
Cancer 153 97.04 Very High Very High Very High
Retinal Neovascularization 4 95.68 Very High Very High Very High
Neuropathic Pain 98 95.12 Very High Very High Very High
Nociception 28 91.00 High High
Hypersensitivity 21 88.88 High High
Cv Unclassified Under Development 1 88.88 High High
INFLAMMATION 126 87.28 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In addition to different types of noxious stimuli, high intensity electrical stimulation of C-fibers also activates ERK in the spinal cord dorsal horn, suggesting that C-fiber recruitment is crucial for release of transmitters that activate ERK centrally in the spinal cord [6,10].
Localization (release) of ERK in spinal cord associated with c fibre, dorsal horn and spinal cord
1) Confidence 0.67 Published 2006 Journal Mol Pain Section Body Doc Link PMC1382249 Disease Relevance 0.50 Pain Relevance 0.67
evidence was published on the combined use of ERK cascade inhibition and PPAR?
Localization (use) of ERK cascade
2) Confidence 0.59 Published 2008 Journal PPAR Research Section Body Doc Link PMC2440494 Disease Relevance 0.65 Pain Relevance 0.11
The activation of ERK pathway and subsequent translocation of NF-kappaB was possibly necessary for the up-regulation TRPC6 induced by Ang II.
Localization (translocation) of ERK
3) Confidence 0.59 Published 2009 Journal Exp. Biol. Med. (Maywood) Section Abstract Doc Link 19546355 Disease Relevance 0.52 Pain Relevance 0.08
Considering the importance of ERK in regulating gene expression, the ERK activation may be required for L-LTP.
Localization (importance) of ERK associated with long-term potentiation
4) Confidence 0.58 Published 2007 Journal Mol Pain Section Body Doc Link PMC2245920 Disease Relevance 0 Pain Relevance 0.84
The signalling pathways were pharmacologically investigated with the pre-administration of adenylyl cyclase (AC), cAMP-dependent protein kinase (PKA), protein kinase Cepsilon (PKCepsilon), and the extracellular signal-related kinase (ERK) inhibitors.
Localization (administration) of ERK
5) Confidence 0.47 Published 2009 Journal Life Sci. Section Body Doc Link 19896488 Disease Relevance 0 Pain Relevance 0
The signalling pathways were pharmacologically investigated with the pre-administration of adenylyl cyclase (AC), cAMP-dependent protein kinase (PKA), protein kinase Cepsilon (PKCepsilon), and the extracellular signal-related kinase (ERK) inhibitors.
Localization (administration) of extracellular signal-related kinase
6) Confidence 0.47 Published 2009 Journal Life Sci. Section Body Doc Link 19896488 Disease Relevance 0 Pain Relevance 0
In normal noncancerous tissue from radical prostatectomy specimens, immunohistochemistry localizes ERK to the cytoplasm of most cells of the prostate including the epithelial, basal, and stromal cells [1,2].
Localization (localizes) of ERK in stromal cells
7) Confidence 0.40 Published 2004 Journal Cell Commun Signal Section Body Doc Link PMC449737 Disease Relevance 0.19 Pain Relevance 0
Our observation that active ERK was localized to angiogenic buds and neovascular outgrowths indicates that altered MKK signaling also may be a factor in retinal neovascularization.
Localization (localized) of ERK associated with retinal neovascularization
8) Confidence 0.36 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2737623 Disease Relevance 0.51 Pain Relevance 0.08
The signal by which nerve injury or disease may lead to microglial activation is unclear, but may relate to acute release of ERK, an enzyme that plays a critical role in intracellular signal transduction and neuronal plasticity.
Localization (release) of ERK in neuronal associated with nervous system injury and disease
9) Confidence 0.28 Published 2010 Journal Mol Pain Section Body Doc Link PMC2845559 Disease Relevance 1.32 Pain Relevance 0.83
Immunoblot analyses for angiotensin II, AT1R, synaptophysin, and phosphorylated forms of ERK, Akt, and STAT3.
Localization (forms) of ERK
10) Confidence 0.26 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.08 Pain Relevance 0.08
ZnR activation induced intracellular release of Ca(2+), as well as phosphorylation of extracellular-regulated kinase and Ca(2+)/calmodulin kinase II.
Localization (release) of extracellular-regulated kinase
11) Confidence 0.22 Published 2009 Journal J. Neurosci. Section Abstract Doc Link 19261885 Disease Relevance 0 Pain Relevance 0.23
and c-Jun (a phosphorylation target of ERK and JNK).
Localization (target) of ERK
12) Confidence 0.18 Published 2004 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC1082887 Disease Relevance 0.17 Pain Relevance 0
Normalization of p-ERK and t-ERK were also conducted against beta-actin, then p-ERK data were quantified as relative intensity of band divided by intensity of t-ERK.
Localization (Normalization) of ERK in band
13) Confidence 0.15 Published 2009 Journal Mol Pain Section Body Doc Link PMC2704199 Disease Relevance 0 Pain Relevance 0
Normalization of p-ERK and t-ERK were also conducted against beta-actin, then p-ERK data were quantified as relative intensity of band divided by intensity of t-ERK.
Localization (Normalization) of ERK in band
14) Confidence 0.15 Published 2009 Journal Mol Pain Section Body Doc Link PMC2704199 Disease Relevance 0 Pain Relevance 0
We have now demonstrated that expression of c-Myc requires phosphorylation and nuclear translocation of ERK, which results in phosphorylation of c-Fos and formation of a specific activator protein (AP)-1 complex.
Localization (translocation) of ERK
15) Confidence 0.13 Published 2010 Journal J. Biol. Chem. Section Abstract Doc Link 20410304 Disease Relevance 0.75 Pain Relevance 0.13
-induced elevation in COX-2 Luciferase (Fig. 5C) and mRNA expression (Fig. 5D) was significantly inhibited by co-treatment of cells with the FP receptor antagonist (AL8810), and chemical inhibitors of PLC (U73122), PKA (4C3MQ), EGFR kinase (AG1478) and ERK1/2 kinase (PD98059), but not the EP2 receptor antagonist (AH6809), EP4 receptor antagonist (ONOAE2227) or PKC inhibitor (GF109203x; Fig. 5C and D, P < 0.05).


Localization (kinase) of ERK1/2 associated with antagonist
16) Confidence 0.12 Published 2008 Journal Molecular and Cellular Endocrinology Section Body Doc Link PMC2694994 Disease Relevance 0 Pain Relevance 0.35
The PGE2-induced elevation in COX-2 Luciferase (Fig. 5A) and mRNA expression (Fig. 5B) was significantly reduced by treatment of FPS cells with the FP receptor antagonist (AL8810), EP2 receptor antagonist (AH6809), EP4 receptor antagonist (ONOAE2227), and chemical inhibitors of PLC (U73122), PKA (4C3MQ), EGFR kinase (AG1478) and ERK1/2 kinase (PD98059), but not the PKC inhibitor (GF109203x; P < 0.05).
Localization (kinase) of ERK1/2 associated with antagonist
17) Confidence 0.12 Published 2008 Journal Molecular and Cellular Endocrinology Section Body Doc Link PMC2694994 Disease Relevance 0 Pain Relevance 0.36
Activated MEK subsequently phosphorylates ERK, which translocates to the nucleus where it activates multiple transcription factors.
Localization (translocates) of ERK in nucleus
18) Confidence 0.08 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2991030 Disease Relevance 0.64 Pain Relevance 0.39
Additional antibodies included rabbit Erk 1/2 (Cell Signaling Technologies) and anti-phospho ERK1/2 purchased from Promega Corporation (Madison, WI).
Localization (purchased) of ERK1/2
19) Confidence 0.07 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2837737 Disease Relevance 0 Pain Relevance 0.03

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