INT171368

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Context Info
Confidence 0.61
First Reported 2002
Last Reported 2010
Negated 3
Speculated 1
Reported most in Body
Documents 14
Total Number 15
Disease Relevance 4.77
Pain Relevance 3.14

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
hepatocyte 4
neurons 4
microglia 4
blood 2
Mapk1 (Mus musculus)
Pain Link Frequency Relevance Heat
addiction 9 100.00 Very High Very High Very High
potassium channel 6 99.48 Very High Very High Very High
cytokine 14 99.20 Very High Very High Very High
Inflammation 65 99.02 Very High Very High Very High
antagonist 71 98.56 Very High Very High Very High
Opioid 69 97.96 Very High Very High Very High
Ventral tegmentum 13 97.72 Very High Very High Very High
Nucleus accumbens 16 97.16 Very High Very High Very High
cocaine 59 94.88 High High
unmyelinated 14 92.72 High High
Disease Link Frequency Relevance Heat
Virus Diseases 94 99.84 Very High Very High Very High
Infection 20 99.68 Very High Very High Very High
Targeted Disruption 55 99.34 Very High Very High Very High
INFLAMMATION 71 99.02 Very High Very High Very High
Reprotox - General 1 3 93.92 High High
Solid Tumor 2 91.20 High High
Glioma 41 90.40 High High
Disease 44 89.08 High High
Starvation 2 88.16 High High
Nervous System Injury 18 82.48 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
However, regulation of the ERK phosphorylation in response to psychostimulants is not as robust in the VTA as in the NAcc.
Regulation (regulation) of Phosphorylation (phosphorylation) of ERK associated with nucleus accumbens and ventral tegmentum
1) Confidence 0.61 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1420315 Disease Relevance 0 Pain Relevance 0.62
-OR down-regulation and an almost complete loss of DSLET-mediated ERK phosphorylation.
Regulation (regulation) of Phosphorylation (phosphorylation) of ERK
2) Confidence 0.41 Published 2002 Journal BMC Pharmacol Section Body Doc Link PMC88976 Disease Relevance 0 Pain Relevance 0.11
Moreover, no change in total ERK expression was observed, concomitantly, with ERK phosphorylation in any of our experiments (data not shown).
Neg (no) Regulation (change) of Phosphorylation (phosphorylation) of ERK
3) Confidence 0.41 Published 2002 Journal BMC Pharmacol Section Body Doc Link PMC88976 Disease Relevance 0 Pain Relevance 0.25
In the present report, DSLET-mediated ERK phosphorylation was unaltered by the presence of the IR or PDGFR antagonists, HNMPA-(AM)3 and tyrosphostin 9, respectively.
Regulation (unaltered) of Phosphorylation (phosphorylation) of ERK associated with antagonist
4) Confidence 0.41 Published 2002 Journal BMC Pharmacol Section Body Doc Link PMC88976 Disease Relevance 0.32 Pain Relevance 0.45
elicited an additive antitumor effect, reduced ERK phosphorylation and
Regulation (effect) of Phosphorylation (phosphorylation) of ERK
5) Confidence 0.35 Published 2008 Journal PPAR Research Section Body Doc Link PMC2440494 Disease Relevance 0.76 Pain Relevance 0.13
Furthermore, we performed an analysis of intracellular signaling mechanisms that could mediate the actions of 3-MT on hTAAR1 expressed in HEK cells. 3-MT caused a rapid and prolonged phosphorylation of Erk2 and CREB only in cells expressing hTAAR1 (Figure 2B,C) thus indicating that a Gs-dependent signaling cascade involving accumulation of cAMP and activation of Erk2 and CREB is likely involved in the action of TAAR1.


Regulation (prolonged) of Phosphorylation (phosphorylation) of Erk2
6) Confidence 0.29 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956650 Disease Relevance 0.08 Pain Relevance 0.11
The expression of Ng induced sustained activation and up-regulation of ERK1/2 phosphorylation by PMA treatment
Regulation (regulation) of Phosphorylation (phosphorylation) of ERK1/2
7) Confidence 0.27 Published 2007 Journal International Journal of Biological Sciences Section Body Doc Link PMC1865092 Disease Relevance 0.20 Pain Relevance 0.08
Therefore, the hepatocyte-specific c-Met conditional knockout mice were also examined for the defects in the Erk1/2 phosphorylation.
Spec (examined) Regulation (defects) of Phosphorylation (phosphorylation) of Erk1/2 in hepatocyte associated with targeted disruption
8) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.19 Pain Relevance 0
Further examination of the effects of suppression of MEK function on a downstream target of ERK phosphorylation, the A-type potassium channel, showed that the ERK-dependent modulation of the A-type currents is significantly reduced in neurons from DN MEK mice compared to littermate wild type controls.


Regulation (target) of Phosphorylation (phosphorylation) of ERK in neurons associated with potassium channel
9) Confidence 0.26 Published 2006 Journal Mol Pain Section Abstract Doc Link PMC1382249 Disease Relevance 0.57 Pain Relevance 0.54
Additional in vivo work combining expression of a CRE-driven LacZ reporter with kinase-specific pharmacological blockade showed that while PKA and ERK inhibition affected CRE-mediated gene expression, the effects of PKA were dependent on ERK phosphorylation (Cancedda et al. 2003).
Regulation (dependent) of Phosphorylation (phosphorylation) of ERK
10) Confidence 0.20 Published 2008 Journal Philosophical Transactions of the Royal Society B: Biological Sciences Section Body Doc Link PMC2674480 Disease Relevance 0 Pain Relevance 0.06
Deletion of c-Met in hepatocytes did not affect the early phosphorylation of Erk1/2 at 6–12 hr following PH but it completely abolished the second peak between 36–48 hr coincidently with a defective progression through G2 phase of cell cycle (Figure 4A).
Neg (not) Regulation (affect) of Phosphorylation (phosphorylation) of Erk1/2 in hepatocytes
11) Confidence 0.16 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.18 Pain Relevance 0
We confirmed the dependence of TNF expression on ERK phosphorylation in LPS-stimulated microglia by inhibiting MAP/ERK kinase (MEK) with UO126 (1 ?
Regulation (dependence) of Phosphorylation (phosphorylation) of ERK in microglia associated with addiction
12) Confidence 0.14 Published 2009 Journal Mol Pain Section Body Doc Link PMC2704199 Disease Relevance 0.06 Pain Relevance 0.08
Following stimulation of neurons with glycine, we observed that ERK 1/2 phosphorylation was not affected by BDV infection (Figure 4A).
Neg (not) Regulation (affected) of Phosphorylation (phosphorylation) of ERK in neurons associated with virus diseases and infection
13) Confidence 0.14 Published 2006 Journal PLoS Pathogens Section Body Doc Link PMC1401496 Disease Relevance 0.76 Pain Relevance 0.18
The effect of sorafenib on phorbol myristate acetate (PMA)-stimulated ERK phosphorylation in peripheral blood lymphocytes (PBLs) was studied using flow cytometry (Strumberg et al 2005).
Regulation (effect) of Phosphorylation (phosphorylation) of ERK in blood
14) Confidence 0.12 Published 2006 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC1661649 Disease Relevance 1.06 Pain Relevance 0
Multiple pathways are involved in the production of this pro-inflammatory cytokine, but our results show a time dependent effect of CBR2 activation on MKP induction (15 min incubation), ERK dephosphorylation (30 min incubation) and decreased TNF (60–120 min incubation), suggesting that p-ERK is instrumental in TNF expression in LPS-stimulated primary microglia.
Regulation (effect) of Phosphorylation (dephosphorylation) of ERK in microglia associated with inflammation and cytokine
15) Confidence 0.06 Published 2009 Journal Mol Pain Section Body Doc Link PMC2704199 Disease Relevance 0.58 Pain Relevance 0.53

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