INT127853

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Context Info
Confidence 0.74
First Reported 2004
Last Reported 2010
Negated 1
Speculated 1
Reported most in Body
Documents 20
Total Number 21
Disease Relevance 5.47
Pain Relevance 7.96

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

endosome (Ephb1) signal transduction (Ephb1) plasma membrane (Ephb1)
cytoplasm (Ephb1)
Anatomy Link Frequency
microglia 2
astrocytes 1
nucleus 1
bands 1
dorsal horn 1
Ephb1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Kinase C 37 100.00 Very High Very High Very High
nMDA receptor 7 100.00 Very High Very High Very High
Glutamate 20 99.98 Very High Very High Very High
withdrawal 10 99.48 Very High Very High Very High
Neuropathic pain 32 99.36 Very High Very High Very High
Antinociceptive 1 99.26 Very High Very High Very High
adenocard 5 99.00 Very High Very High Very High
tolerance 15 98.80 Very High Very High Very High
long-term potentiation 74 98.44 Very High Very High Very High
Morphine 24 98.44 Very High Very High Very High
Disease Link Frequency Relevance Heat
Neuropathic Pain 58 99.36 Very High Very High Very High
Apoptosis 112 97.84 Very High Very High Very High
Attention Deficit Hyperactivity Disorder 7 96.40 Very High Very High Very High
Necrosis 4 96.36 Very High Very High Very High
Cancer 10 96.00 Very High Very High Very High
Urological Neuroanatomy 3 93.88 High High
Mycobacterium Infection 1 92.40 High High
Ganglion Cysts 60 92.24 High High
Body Weight 2 90.04 High High
Cystitis 6 89.40 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
AIM: To investigate whether activation and translocation of extracellular signal-regulated kinase (ERK) is involved in the induction and maintenance of neuropathic pain, and effects of activation and translocation of ERK on expression of pCREB and Fos in the chronic neuropathic pain.
Localization (translocation) of ERK associated with neuropathic pain
1) Confidence 0.74 Published 2005 Journal Acta Pharmacol. Sin. Section Abstract Doc Link 15960884 Disease Relevance 0.35 Pain Relevance 0.31
Interruption of ERK signalling may occur by (1) hyperphosphorylation of Raf and MEK 1 and 2, (2) dephosphorylation of aminoacidic residues of ERK and (3) sequestration of ERK in the nucleus.
Localization (sequestration) of ERK in nucleus
2) Confidence 0.73 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644492 Disease Relevance 0 Pain Relevance 0
In this case, ERK phosphorylation was found in the cytoplasm and nuclei of spinal neurons [31, 62, 102, 117] but also in glial cells, including microglia and astrocytes [31, 63, 117].
Localization (found) of ERK in astrocytes
3) Confidence 0.69 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644492 Disease Relevance 0.67 Pain Relevance 0.49
The main localization of ERK-P in Bungner's bands observed in this study is in accordance with these findings.
Localization (localization) of ERK in bands
4) Confidence 0.66 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1501035 Disease Relevance 0.17 Pain Relevance 0.07
AIM: To investigate whether activation and translocation of extracellular signal-regulated kinase (ERK) is involved in the induction and maintenance of neuropathic pain, and effects of activation and translocation of ERK on expression of pCREB and Fos in the chronic neuropathic pain.
Spec (whether) Localization (translocation) of ERK associated with neuropathic pain
5) Confidence 0.65 Published 2005 Journal Acta Pharmacol. Sin. Section Abstract Doc Link 15960884 Disease Relevance 0.34 Pain Relevance 0.30
Double immunofluorescence staining showed that p-ERK and p-CREB were only located in neurons but not in glial cells in the spinal dorsal horn after LTP induction.
Neg (not) Localization (located) of ERK in dorsal horn associated with spinal dorsal horn and long-term potentiation
6) Confidence 0.63 Published 2006 Journal J. Neurosci. Res. Section Abstract Doc Link 16902997 Disease Relevance 0.08 Pain Relevance 0.94
OBJECTIVE: Identify time-course, localization, and expression of pERK.
Localization (localization) of pERK
7) Confidence 0.63 Published 2006 Journal Spine Section Body Doc Link 16508545 Disease Relevance 0.19 Pain Relevance 0
A 7-d treatment with morphine induced tolerance to the antinociceptive effect and increased phosphorylated ERK localized in astrocytes and phosphorylated p38 enriched in microglia, both effects being inhibited by blocking CGRP receptors.
Localization (localized) of ERK in microglia associated with tolerance, antinociceptive, calcitonin gene-related peptide and morphine
8) Confidence 0.54 Published 2009 Journal FASEB J. Section Abstract Doc Link 19299480 Disease Relevance 0.07 Pain Relevance 1.63
Double immunostaining showed that after LTP induction, most pERK was co-localized with pCREB.
Localization (localized) of pERK
9) Confidence 0.52 Published 2009 Journal Neurosci Bull Section Body Doc Link 19784086 Disease Relevance 0.06 Pain Relevance 0
We observed significant increases in the phosphorylation of JNK and ERK (normalized to total protein) in 2CLP monolayers compared to sham (Figure 9).
Localization (normalized) of ERK
10) Confidence 0.44 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2892473 Disease Relevance 0 Pain Relevance 0
The water extracts of adlay seeds also enhanced extracellular signal-regulated protein kinase (ERK) 1/2 phosphorylation and protein kinase C (PKC)-alpha translocation from cytosolic to particulate fractions in uteri.
Localization (translocation) of ERK associated with kinase c
11) Confidence 0.38 Published 2005 Journal J. Toxicol. Environ. Health Part A Section Abstract Doc Link 16076766 Disease Relevance 0.39 Pain Relevance 0.23
These results suggest that PF's analgesic effect is possibly mediated by adenosine A(1) receptor by inhibiting CRD-evoked glutamate release and the NMDA receptor dependent ERK signaling.
Localization (release) of ERK associated with glutamate, adenocard, nmda receptor and analgesic
12) Confidence 0.35 Published 2009 Journal Pharmacol. Biochem. Behav. Section Abstract Doc Link 19664651 Disease Relevance 0.37 Pain Relevance 1.15
In contrast, PKC inhibitor calphostin C reduced the withdrawal-triggered rise in pCREB, pERK(1/2), TH expression and corticosterone secretion.
Localization (secretion) of pERK associated with kinase c and withdrawal
13) Confidence 0.34 Published 2009 Journal J. Neurochem. Section Abstract Doc Link 19545278 Disease Relevance 0.16 Pain Relevance 1.13
The promoter region of NOS I gene contains putative cis-elements of binding sites for cAMP response element (CREB), C/EBP and c-Myc [39,40], which are candidates for ERK nuclear targeting in the mediation of gene transcription.
Localization (targeting) of ERK
14) Confidence 0.30 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2848001 Disease Relevance 0.24 Pain Relevance 0.10
In this case, ERK phosphorylation was found in the cytoplasm and nuclei of spinal neurons [31, 62, 102, 117] but also in glial cells, including microglia and astrocytes [31, 63, 117].
Localization (found) of ERK in microglia
15) Confidence 0.23 Published 2007 Journal Current Neuropharmacology Section Body Doc Link PMC2644492 Disease Relevance 0.67 Pain Relevance 0.49
SP is released through a very complex process involving some important intracellular effectors, such as extracellular calcium influx, 1,4,5-inositol trisphosphate-induced calcium release, the activation of extracellular signal-regulated kinase (ERK), cyclooxygenases (COXs) and prostaglandins, and the cyclic AMP-dependent protein kinase A (PKA) from primary afferent neurons to convey information about various noxious stimuli [3-6].
Localization (release) of ERK in afferent neurons associated with substance p
16) Confidence 0.21 Published 2007 Journal Mol Pain Section Body Doc Link PMC2235838 Disease Relevance 0.41 Pain Relevance 0.65
The following primary antibodies were used: rabbit anti-ERK, mouse anti-phospho ERK, mouse anti-Bcl-2, rabbit anti-Bax (Assay Designs, Ann Arbor, MI, USA), mouse anti-SERCA2a, mouse anti-NCX (Affinity Bioreagents, Rockford, IL, USA), and mouse anti-?
Localization (used) of ERK
17) Confidence 0.15 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2824862 Disease Relevance 0.12 Pain Relevance 0
The following primary antibodies were used: rabbit anti-ERK, mouse anti-phospho ERK, mouse anti-Bcl-2, rabbit anti-Bax (Assay Designs, Ann Arbor, MI, USA), mouse anti-SERCA2a, mouse anti-NCX (Affinity Bioreagents, Rockford, IL, USA), and mouse anti-?
Localization (anti) of ERK
18) Confidence 0.15 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2824862 Disease Relevance 0.12 Pain Relevance 0
The following primary antibodies were used: rabbit anti-ERK, mouse anti-phospho ERK, mouse anti-Bcl-2, rabbit anti-Bax (Assay Designs, Ann Arbor, MI, USA), mouse anti-SERCA2a, mouse anti-NCX (Affinity Bioreagents, Rockford, IL, USA), and mouse anti-?
Localization (used) of ERK
19) Confidence 0.15 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2824862 Disease Relevance 0.12 Pain Relevance 0
B binding activity, ERK and p-38-dependent cytochrome c release, and caspase-3 activation [22-24].
Localization (release) of ERK
20) Confidence 0.14 Published 2004 Journal Comp Hepatol Section Body Doc Link PMC516785 Disease Relevance 0.72 Pain Relevance 0

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