INT53491

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Context Info
Confidence 0.57
First Reported 1994
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 28
Total Number 30
Disease Relevance 14.20
Pain Relevance 6.90

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

cytosol (Jun) nucleus (Jun) DNA binding (Jun)
transcription factor binding (Jun)
Anatomy Link Frequency
T cells 2
hepatocytes 1
brain 1
Jun (Mus musculus)
Pain Link Frequency Relevance Heat
Morphine 11 100.00 Very High Very High Very High
cINOD 62 99.74 Very High Very High Very High
COX2 8 99.58 Very High Very High Very High
COX-2 inhibitor 14 99.48 Very High Very High Very High
tolerance 7 99.20 Very High Very High Very High
agonist 84 99.18 Very High Very High Very High
adenocard 4 98.92 Very High Very High Very High
Inflammation 404 97.92 Very High Very High Very High
Inflammatory mediators 23 97.36 Very High Very High Very High
Enkephalin 2 96.80 Very High Very High Very High
Disease Link Frequency Relevance Heat
Repression 15 100.00 Very High Very High Very High
Fibromyalgia 1 99.12 Very High Very High Very High
Shock 7 98.92 Very High Very High Very High
Stress 23 98.68 Very High Very High Very High
Wound Healing 31 98.52 Very High Very High Very High
Pneumonia 1 98.48 Very High Very High Very High
Apoptosis 109 98.44 Very High Very High Very High
Burns 222 98.28 Very High Very High Very High
Injury 160 98.20 Very High Very High Very High
Urological Neuroanatomy 33 98.06 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
METHODS: Mouse hepatocytes and C57BL/6 mice were administered a toxic dose of APAP with or without SP600125, a chemical c-jun N-terminal kinase (JNK) inhibitor.
Negative_regulation (inhibitor) of c-jun in hepatocytes
1) Confidence 0.57 Published 2006 Journal Gastroenterology Section Body Doc Link 16831600 Disease Relevance 0.19 Pain Relevance 0
Based on our results, we propose that the inhibition of AP-1 activity by COX-2 inhibitors NS-398 or piroxicam may occur by a mechanism that is independent of COX-2.
Negative_regulation (inhibition) of AP-1 associated with cox-2 inhibitor
2) Confidence 0.56 Published 2003 Journal J. Biol. Chem. Section Abstract Doc Link 12433932 Disease Relevance 0.13 Pain Relevance 0.18
Further study revealed that the inhibitor of c-Jun N-terminal kinase - mitogen-activated protein kinase (JNK-MAPK), SP600125 (0.1 microM), reversed the imipramine-induced suppression of GR function, whereas the inhibitor of extracellular signal-regulated kinase (ERK)-MAPK, PD 98059 (15 microM), potentiated the antidepressant action.
Negative_regulation (inhibitor) of c-Jun associated with antidepressant
3) Confidence 0.42 Published 2008 Journal J. Physiol. Pharmacol. Section Abstract Doc Link 18441395 Disease Relevance 0.09 Pain Relevance 0.29
NS-398 and piroxicam suppress UVB-induced activator protein 1 activity by mechanisms independent of cyclooxygenase-2.
Negative_regulation (suppress) of activator protein 1 associated with cox2
4) Confidence 0.41 Published 2003 Journal J. Biol. Chem. Section Title Doc Link 12433932 Disease Relevance 0.16 Pain Relevance 0.21
Immediate-release morphine decreased in both; former users required more (P = 0.0006).
Negative_regulation (decreased) of Immediate-release morphine associated with morphine
5) Confidence 0.34 Published 2000 Journal J Pain Symptom Manage Section Abstract Doc Link 10799793 Disease Relevance 0.92 Pain Relevance 1.47
suggest that the inhibition of TPA-induced AP-1 activity and cell
Negative_regulation (inhibition) of AP-1
6) Confidence 0.25 Published 2004 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC1082887 Disease Relevance 0.17 Pain Relevance 0
have been shown to inhibit TPA-induced AP-1 transcriptional
Negative_regulation (inhibit) of AP-1
7) Confidence 0.25 Published 2004 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC1082887 Disease Relevance 0.39 Pain Relevance 0
activation of JNK2 in response to TPA, thereby delaying AP-1
Negative_regulation (delaying) of AP-1
8) Confidence 0.25 Published 2004 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC1082887 Disease Relevance 0.26 Pain Relevance 0
NSAIDs are able to inactivate the transcription NF-kB and activator protein-1 (AP-1), critically involved in the induction of multiple inflammatory gene products involved in the inflammatory response (i.e. iNOS, TNF-?).
Negative_regulation (inactivate) of activator protein-1 associated with inflammatory response, inflammation and cinod
9) Confidence 0.22 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3000390 Disease Relevance 0.61 Pain Relevance 0.48
NSAIDs are able to inactivate the transcription NF-kB and activator protein-1 (AP-1), critically involved in the induction of multiple inflammatory gene products involved in the inflammatory response (i.e. iNOS, TNF-?).
Negative_regulation (inactivate) of AP-1 associated with inflammatory response, inflammation and cinod
10) Confidence 0.22 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3000390 Disease Relevance 0.61 Pain Relevance 0.48
Many immediate early genes such as Fos, Jun and Early Growth Response isoforms were down-regulated although others associated with stress such as glucocorticoid responsive genes were up-regulated.
Negative_regulation (regulated) of immediate early associated with stress
11) Confidence 0.22 Published 2010 Journal BMC Neurosci Section Abstract Doc Link PMC2939656 Disease Relevance 0.45 Pain Relevance 0.06
Ginsenosides attenuate methamphetamine-induced behavioral side effects in mice via activation of adenosine A2A receptors: possible involvements of the striatal reduction in AP-1 DNA binding activity and proenkephalin gene expression.
Spec (possible) Negative_regulation (reduction) of AP-1 associated with adenocard and enkephalin
12) Confidence 0.17 Published 2005 Journal Behav. Brain Res. Section Title Doc Link 15680202 Disease Relevance 0 Pain Relevance 0.46
The shift in the composition of the AP-1 complex may be mediated by inhibition of JNK activity because the western blot analysis indicated that phospho-c-Jun decreases in the cytoplasm after VIP treatment (Fig. 5d).


Negative_regulation (decreases) of phospho-c-Jun
13) Confidence 0.15 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1257432 Disease Relevance 0.68 Pain Relevance 0.34
-mediated repression of AP-1-regulated genes [58].
Negative_regulation (repression) of AP-1-regulated associated with repression
14) Confidence 0.14 Published 2008 Journal PPAR Research Section Body Doc Link PMC2443396 Disease Relevance 0.22 Pain Relevance 0.12
It has been also demonstrated that the FERM (band 4.1, ezrin, radixin, moesin) domain of PTPH1 is necessary for the inhibition of Mek, Erk, Jnk and AP-1 and also for localization of the phosphatase on the plasma membrane of Jurkat T cells [14].
Negative_regulation (inhibition) of AP-1 in T cells
15) Confidence 0.13 Published 2010 Journal J Inflamm (Lond) Section Body Doc Link PMC2873500 Disease Relevance 0.16 Pain Relevance 0.03
Many immediate early genes such as Fos, Jun and Early Growth Response isoforms were down-regulated although others associated with stress such as glucocorticoid responsive genes were up-regulated.
Negative_regulation (regulated) of Jun associated with stress
16) Confidence 0.11 Published 2010 Journal BMC Neurosci Section Abstract Doc Link PMC2939656 Disease Relevance 0.45 Pain Relevance 0.06
ligands may be due to their ability to inhibit the activity of key transcription factors such as activator protein-1 (AP-1) and nuclear factor ?
Negative_regulation (inhibit) of activator protein-1
17) Confidence 0.11 Published 2006 Journal Arthritis Res Ther Section Body Doc Link PMC1526548 Disease Relevance 0.70 Pain Relevance 0.49
ligands may be due to their ability to inhibit the activity of key transcription factors such as activator protein-1 (AP-1) and nuclear factor ?
Negative_regulation (inhibit) of AP-1
18) Confidence 0.11 Published 2006 Journal Arthritis Res Ther Section Body Doc Link PMC1526548 Disease Relevance 0.70 Pain Relevance 0.49
Since NCoA6 is known to play an important role in c-Jun signaling [Ko et al., 2000; Lee et al., 2000; Mahajan et al., 2002], the impaired wound healing phenotype of NCoA6(NRC)+/- mice can be explained, at least in part, by a reduction in c-Jun activity.
Negative_regulation (reduction) of c-Jun associated with wound healing
19) Confidence 0.10 Published 2008 Journal Nuclear Receptor Signaling Section Body Doc Link PMC2254332 Disease Relevance 0.48 Pain Relevance 0
In the short time following its discovery, NCoA6 has emerged as an important coactivator not only for NRs, but also for a number of other well known transcription factors such as c-Fos, c-Jun, CREB, NF-kB, ATF-2, heat shock factors, E2F-1, SRF, Rb, p53 and Stat2 [Goo et al., 2004; Hong et al., 2004a; Hong et al., 2004b; Ko et al., 2000; Kong et al., 2003; Lee et al., 1999; Lee et al., 2000; Mahajan et al., 2007; Mahajan et al., 2002; Mahajan and Samuels, 2000; Mahajan and Samuels, 2005].
Negative_regulation (number) of c-Jun associated with shock
20) Confidence 0.10 Published 2008 Journal Nuclear Receptor Signaling Section Body Doc Link PMC2254332 Disease Relevance 0.39 Pain Relevance 0

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