INT6660

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Context Info
Confidence 0.69
First Reported 1992
Last Reported 2010
Negated 1
Speculated 5
Reported most in Abstract
Documents 148
Total Number 155
Disease Relevance 67.58
Pain Relevance 29.73

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
skin 4
macrophages 3
brain 3
apoptotic cell 3
liver 3
Jun (Mus musculus)
Pain Link Frequency Relevance Heat
adenocard 10 100.00 Very High Very High Very High
tramadol 7 100.00 Very High Very High Very High
Anterior cingulate cortex 486 99.84 Very High Very High Very High
ischemia 108 99.84 Very High Very High Very High
cINOD 178 99.74 Very High Very High Very High
Inflammation 1173 99.72 Very High Very High Very High
agonist 194 99.70 Very High Very High Very High
Paracetamol 48 99.56 Very High Very High Very High
nMDA receptor 46 99.44 Very High Very High Very High
Morphine 38 99.42 Very High Very High Very High
Disease Link Frequency Relevance Heat
Stress 362 100.00 Very High Very High Very High
Death 194 100.00 Very High Very High Very High
Shock 63 100.00 Very High Very High Very High
Cancer 827 99.98 Very High Very High Very High
Rheumatoid Arthritis 298 99.90 Very High Very High Very High
Convulsion 52 99.90 Very High Very High Very High
Cv Unclassified Under Development 35 99.84 Very High Very High Very High
Injury 219 99.78 Very High Very High Very High
INFLAMMATION 1373 99.72 Very High Very High Very High
Breast Cancer 135 99.70 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In the present studies, we determined that exposure to necrogenic doses of acetaminophen (APAP) was associated with increased AP-1 DNA binding activity in mouse liver.
Positive_regulation (increased) of AP-1 in liver associated with paracetamol
1) Confidence 0.69 Published 1996 Journal Res. Commun. Mol. Pathol. Pharmacol. Section Abstract Doc Link 8827825 Disease Relevance 0.55 Pain Relevance 0.53
AP-1 is usually expressed at low basal cellular levels, but can be up-regulated by a variety of exogenous stimuli which results in synthesis of Fos and Jun proteins and increased AP-1 DNA binding activity.
Positive_regulation (increased) of AP-1
2) Confidence 0.69 Published 1996 Journal Res. Commun. Mol. Pathol. Pharmacol. Section Abstract Doc Link 8827825 Disease Relevance 0.35 Pain Relevance 0.34
Some of the compounds were strong inhibitors of the activation of AP-1.
Positive_regulation (activation) of AP-1
3) Confidence 0.69 Published 2008 Journal BMC Pharmacol Section Body Doc Link PMC2632638 Disease Relevance 0 Pain Relevance 0
Activation of AP-1 can be inhibited by numerous natural product polyphenols such as resveratrol, curcumin, epigallocatechin gallate and theaflavins [6,15,16].
Positive_regulation (Activation) of AP-1
4) Confidence 0.69 Published 2008 Journal BMC Pharmacol Section Body Doc Link PMC2632638 Disease Relevance 0.31 Pain Relevance 0.09
Gel-shift assays showed that enoxacin-induced convulsions resulted in increases in nuclear activator protein 1 (AP-1) DNA- and cyclic AMP responsive element (CRE)-binding activities in the cerebral cortex and hippocampus, but not in other regions, such as the cerebellum and thalamus.
Positive_regulation (increases) of AP-1 in cerebellum associated with convulsion, thalamus, hippocampus and cerebral cortex
5) Confidence 0.68 Published 1999 Journal Neuropharmacology Section Abstract Doc Link 10340309 Disease Relevance 0.67 Pain Relevance 0.30
CPS itself does not affect the DNA-binding ability of NF-kappaB but it prevents IkappaB kinase activation and IkappaBalpha degradation in a dose-dependent manner, without inhibiting the activation of the mitogen-activated protein kinases, p38, extracellular regulated kinase and c-Jun N-terminal protein kinase.
Positive_regulation (activation) of c-Jun associated with qutenza
6) Confidence 0.67 Published 2002 Journal Eur. J. Immunol. Section Abstract Doc Link 12115659 Disease Relevance 0.25 Pain Relevance 0.49
Combined TNFalpha and NMDA stimulation results in a transient increase in activity of extracellular signal-regulated kinases (ERKs) and c-Jun N-terminal kinases (JNKs).
Positive_regulation (increase) of c-Jun
7) Confidence 0.67 Published 2007 Journal J. Neurochem. Section Abstract Doc Link 17241124 Disease Relevance 0.82 Pain Relevance 0.77
In support of plastic changes in the ACC after injury, activity-dependent immediate early genes, such as c-fos, Egr1, adenosine 3',5'-monophosphate response element binding protein (CREB) are activated in the ACC neurons after tissue inflammation or amputation [41,57].
Positive_regulation (activated) of immediate early in ACC neurons associated with adenocard, inflammation, injury, amputation and anterior cingulate cortex
8) Confidence 0.67 Published 2007 Journal Mol Pain Section Body Doc Link PMC1904186 Disease Relevance 1.17 Pain Relevance 0.66
Interestingly, the induction of immediate early genes c-Fos and Egr-1 which can function as sensors for duration of Erk1/2 signaling [20] was reduced in c-Met mutant mice, particularly at the later time points of liver regeneration (Figure S3).
Positive_regulation (induction) of immediate early in liver
9) Confidence 0.67 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.05 Pain Relevance 0
In general, p38 MAPKs are activated by many stimuli, including cytokines, hormones, ligands for G protein-coupled receptors, and elevated levels of these cytokines are associated with asthma.
Positive_regulation (activated) of AP associated with asthma and cytokine
10) Confidence 0.67 Published 2008 Journal J Occup Med Toxicol Section Body Doc Link PMC2259400 Disease Relevance 0.85 Pain Relevance 0.33
UVB significantly increased AP-1 activity in Cox-2(-/-) fibroblasts transfected with an AP-1 luciferase reporter gene, and this increase was blocked by NS-389 or piroxicam.
Positive_regulation (increased) of AP-1 in fibroblasts
11) Confidence 0.66 Published 2003 Journal J. Biol. Chem. Section Abstract Doc Link 12433932 Disease Relevance 0.16 Pain Relevance 0.20
However, in the present study we found that both piroxicam, a general COX inhibitor, and NS-398, a COX-2 selective inhibitor, effectively suppressed the activation of transcription factor activator protein 1 (AP-1) induced by ultraviolet B (UVB) or 12-O-tetradecanoylphorbol-13-acetate in mouse epidermal JB6 cells.
Positive_regulation (activation) of AP-1
12) Confidence 0.66 Published 2003 Journal J. Biol. Chem. Section Abstract Doc Link 12433932 Disease Relevance 0.18 Pain Relevance 0.18
DEM, APAP, and CCl(4) increased c-jun and c-fos mRNA levels, together with an increase in AP-1 binding; BSO failed to induce AP-1 despite an increase in c-fos.
Neg (failed) Positive_regulation (induce) of AP-1
13) Confidence 0.65 Published 2000 Journal Hepatology Section Abstract Doc Link 10915739 Disease Relevance 0.29 Pain Relevance 0.08
The results showed that c-fos and c-jun were induced in ischemia-reperfusion myocardium at endcardiopulmonary bypass.
Positive_regulation (induced) of c-jun in myocardium associated with ischemia
14) Confidence 0.64 Published 2010 Journal Virol J Section Body Doc Link PMC2976746 Disease Relevance 0.76 Pain Relevance 0.74
These results suggest that the increased nuclear AP-1 DNA- and CRE-binding activities in the cerebral cortex and hippocampus induced by quinolones with BPAA correlated with seizure activities and that these brain regions play pivotal roles in quinolone-induced convulsions.
Positive_regulation (increased) of AP-1 DNA in brain associated with convulsion, hippocampus and cerebral cortex
15) Confidence 0.59 Published 1999 Journal Neuropharmacology Section Abstract Doc Link 10340309 Disease Relevance 0.82 Pain Relevance 0.30
Likewise, phorbol ester-induced activation of activator protein-1 (AP-1) was abolished by capsaicin pretreatment.
Positive_regulation (activation) of AP-1 associated with qutenza
16) Confidence 0.59 Published 2001 Journal Cancer Lett. Section Abstract Doc Link 11179825 Disease Relevance 0.17 Pain Relevance 0.58
Capsaicin suppresses phorbol ester-induced activation of NF-kappaB/Rel and AP-1 transcription factors in mouse epidermis.
Positive_regulation (activation) of AP-1 in epidermis associated with qutenza
17) Confidence 0.59 Published 2001 Journal Cancer Lett. Section Title Doc Link 11179825 Disease Relevance 0.19 Pain Relevance 0.70
Likewise, phorbol ester-induced activation of activator protein-1 (AP-1) was abolished by capsaicin pretreatment.
Positive_regulation (activation) of activator protein-1 associated with qutenza
18) Confidence 0.59 Published 2001 Journal Cancer Lett. Section Abstract Doc Link 11179825 Disease Relevance 0.17 Pain Relevance 0.58
Since altered transactivation of NF-kappaB and AP-1 has been implicated for neoplastic transformation and progression, the suppression of these transcription factors by capsaicin may account for its previously reported chemopreventive effects on mouse skin tumorigenesis as well as inflammation.
Positive_regulation (transactivation) of AP-1 in skin associated with inflammation and qutenza
19) Confidence 0.59 Published 2001 Journal Cancer Lett. Section Abstract Doc Link 11179825 Disease Relevance 0.25 Pain Relevance 0.59
However, in the present study we found that both piroxicam, a general COX inhibitor, and NS-398, a COX-2 selective inhibitor, effectively suppressed the activation of transcription factor activator protein 1 (AP-1) induced by ultraviolet B (UVB) or 12-O-tetradecanoylphorbol-13-acetate in mouse epidermal JB6 cells.
Positive_regulation (activation) of activator protein 1
20) Confidence 0.58 Published 2003 Journal J. Biol. Chem. Section Abstract Doc Link 12433932 Disease Relevance 0.18 Pain Relevance 0.18

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