INT88498

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Context Info
Confidence 0.82
First Reported 2000
Last Reported 2009
Negated 0
Speculated 0
Reported most in Abstract
Documents 14
Total Number 14
Disease Relevance 6.94
Pain Relevance 7.10

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

cytosol (Nfkbia) plasma membrane (Nfkbia) nucleus (Nfkbia)
enzyme binding (Nfkbia) protein complex (Nfkbia) cytoplasm (Nfkbia)
Anatomy Link Frequency
spinal cord 2
macrophage 1
Hepa 1-6 1
PC-3 1
nucleus 1
Nfkbia (Mus musculus)
Pain Link Frequency Relevance Heat
Paracetamol 11 99.76 Very High Very High Very High
cytokine 2 99.76 Very High Very High Very High
Hyperalgesia 10 99.28 Very High Very High Very High
Spinal cord 6 99.08 Very High Very High Very High
qutenza 30 99.00 Very High Very High Very High
Inflammation 38 97.36 Very High Very High Very High
Sciatic nerve 2 92.00 High High
Analgesic 16 88.68 High High
agonist 12 84.60 Quite High
Intracerebroventricular 5 75.00 Quite High
Disease Link Frequency Relevance Heat
Pressure And Volume Under Development 15 99.50 Very High Very High Very High
Necrosis 9 99.50 Very High Very High Very High
Cancer 10 99.32 Very High Very High Very High
Hyperalgesia 12 99.28 Very High Very High Very High
INFLAMMATION 39 97.36 Very High Very High Very High
Nociception 2 95.60 Very High Very High Very High
Neuropathic Pain 1 92.44 High High
Reprotox - General 1 10 91.04 High High
Hepatocellular Cancer 1 80.92 Quite High
Toxicity 2 72.88 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
PEA prevented IkB-alpha degradation and NF-kappaB nuclear translocation, confirming the involvement of this transcriptional factor in the control of peripheral inflammation.
Protein_catabolism (degradation) of IkB-alpha associated with inflammation
1) Confidence 0.82 Published 2007 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 17565008 Disease Relevance 0.50 Pain Relevance 0.50
Treatment of Hepa 1-6 cells with H(2)O(2) was sufficient for NF-kappaB activation and IkappaBalpha degradation, and APAP was able to block both of these events.
Protein_catabolism (degradation) of IkappaBalpha in Hepa 1-6 associated with paracetamol
2) Confidence 0.76 Published 2000 Journal Toxicol. Sci. Section Abstract Doc Link 10828269 Disease Relevance 0.15 Pain Relevance 0.89
PEA attenuated the development of carrageenan-induced paw edema, we evaluated inhibitor kappaB-alpha (I kappa B-alpha) degradation and nuclear factor-kappaB (NF-kappaB) p65 activation in the cytosolic or nuclear extracts from spinal cord tissue.
Protein_catabolism (degradation) of kappaB-alpha in spinal cord associated with pressure and volume under development and spinal cord
3) Confidence 0.72 Published 2007 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 17565008 Disease Relevance 0.52 Pain Relevance 0.55
PEA attenuated the development of carrageenan-induced paw edema, we evaluated inhibitor kappaB-alpha (I kappa B-alpha) degradation and nuclear factor-kappaB (NF-kappaB) p65 activation in the cytosolic or nuclear extracts from spinal cord tissue.
Protein_catabolism (degradation) of I kappa B-alpha in spinal cord associated with pressure and volume under development and spinal cord
4) Confidence 0.72 Published 2007 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 17565008 Disease Relevance 0.52 Pain Relevance 0.54
To investigate the mechanism by which PEA attenuated hyperalgesia, we evaluated inhibitory kB-alpha (IkB-alpha) degradation and p65 nuclear factor kB (NF-kappaB) activation in DRG.
Protein_catabolism (degradation) of IkB-alpha in DRG associated with hyperalgesia
5) Confidence 0.66 Published 2009 Journal Eur. J. Pharmacol. Section Abstract Doc Link 19386271 Disease Relevance 0.68 Pain Relevance 0.89
PEA prevented IkB-alpha degradation and p65 NF-kappaB nuclear translocation, confirming the involvement of this transcriptional factor in the control of peripheral hyperalgesia.
Protein_catabolism (degradation) of IkB-alpha associated with hyperalgesia
6) Confidence 0.66 Published 2009 Journal Eur. J. Pharmacol. Section Abstract Doc Link 19386271 Disease Relevance 0.61 Pain Relevance 0.81
Similarly, the study by Singer et al. showed that p38 MAPK and NF-kappa B may affect COX-2 expression in human airway myocytes via separate signaling pathways given the fact that SB203580 did not affect cytokine-stimulated IkappaBalpha degradation and NF-kappa B nuclear binding activity [23].
Protein_catabolism (degradation) of IkappaBalpha in myocytes associated with cytokine
7) Confidence 0.35 Published 2008 Journal Respir Res Section Body Doc Link PMC2270828 Disease Relevance 0.18 Pain Relevance 0.05
Taken together, capsaicin inhibits proteasome activity which suppressed the degradation of IkappaBalpha, preventing the activation of NF-kappaB.
Protein_catabolism (degradation) of IkappaBalpha associated with qutenza
8) Confidence 0.34 Published 2006 Journal Cancer Res. Section Abstract Doc Link 16540674 Disease Relevance 0.54 Pain Relevance 0.88
In further studies, capsaicin inhibited tumor necrosis factor-alpha-stimulated degradation of IkappaBalpha in PC-3 cells, which was associated with the inhibition of proteasome activity.
Protein_catabolism (degradation) of IkappaBalpha in PC-3 associated with necrosis, qutenza and cancer
9) Confidence 0.22 Published 2006 Journal Cancer Res. Section Abstract Doc Link 16540674 Disease Relevance 0.56 Pain Relevance 0.87
In the present study, topical application of capsaicin onto dorsal skin of female ICR mice strongly suppressed phorbol ester-stimulated activation of NF-kappaB via blockade of IkappaB-alpha degradation with subsequent inhibition of nuclear translocation of the functionally active NF-kappaB subunit, p65.
Protein_catabolism (degradation) of IkappaB-alpha in skin associated with qutenza
10) Confidence 0.14 Published 2001 Journal Cancer Lett. Section Abstract Doc Link 11179825 Disease Relevance 0.18 Pain Relevance 0.57
Furthermore, EAAD suppressed LPS-induced phosphorylation of p38 MAPK and extracellular-signal regulated kinases 1/2 (ERK1/2), I-kappaBalpha degradation, and NF-kappaB activation in RAW 264.7 cells.
Protein_catabolism (degradation) of I-kappaBalpha in RAW 264
11) Confidence 0.08 Published 2007 Journal Pharmacol. Res. Section Abstract Doc Link 17229575 Disease Relevance 1.02 Pain Relevance 0.25
These results suggest that EAAD has the inhibitory effects on LPS-induced TNF-alpha, NO and PGE(2) production, and expression of iNOS and COX-2 in macrophage through blockade in the phosphorylation of MAPKs, following I-kappaBalpha degradation and NF-kappaB activation.
Protein_catabolism (degradation) of I-kappaBalpha in macrophage
12) Confidence 0.08 Published 2007 Journal Pharmacol. Res. Section Abstract Doc Link 17229575 Disease Relevance 0.67 Pain Relevance 0.06
Furthermore, MEXS inhibited nuclear factor kappa B (NF-kappaB) DNA binding activity and the translocation of NF-kappaB to the nucleus by blocking the degradation of inhibitor of kappa B-alpha (IkappaB-alpha).
Protein_catabolism (degradation) of IkappaB-alpha in nucleus
13) Confidence 0.02 Published 2005 Journal Biol. Pharm. Bull. Section Abstract Doc Link 15635170 Disease Relevance 0.66 Pain Relevance 0.23
The NF-kappaB complex was composed of p50 and p65 subunits and its activation required inhibitor of NF-kappaBalpha degradation.
Protein_catabolism (degradation) of NF-kappaBalpha
14) Confidence 0.02 Published 2007 Journal J. Rheumatol. Section Body Doc Link 17896809 Disease Relevance 0.14 Pain Relevance 0

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