INT93401

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Context Info
Confidence 0.46
First Reported 2001
Last Reported 2005
Negated 3
Speculated 1
Reported most in Abstract
Documents 11
Total Number 12
Disease Relevance 3.89
Pain Relevance 2.70

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)
Nfkbia (Rattus norvegicus)
Pain Link Frequency Relevance Heat
diclofenac 4 99.98 Very High Very High Very High
aspirin 2 99.84 Very High Very High Very High
Inflammation 12 95.68 Very High Very High Very High
Migraine 9 94.60 High High
Central nervous system 12 93.60 High High
cINOD 4 93.04 High High
Multiple sclerosis 8 86.32 High High
qutenza 6 78.08 Quite High
COX-2 inhibitor 2 76.28 Quite High
Inflammatory response 1 63.16 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 15 95.68 Very High Very High Very High
Headache 9 94.60 High High
Stomach Cancer 3 94.16 High High
Skin Cancer 10 93.92 High High
Colon Cancer 4 90.04 High High
Demyelinating Disease 8 86.32 High High
Disease 8 79.64 Quite High
Glioma 6 79.08 Quite High
Pressure And Volume Under Development 3 73.84 Quite High
Cancer 2 65.04 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Investigating the molecular mechanisms by which parthenolide prevents iNOS/NO synthesis, we found that parthenolide inhibits the activation of p42/44 mitogen-activated protein kinase (MAPK), but not IkBalpha (IkappaBalpha) degradation or nuclear factor-kappaB (NF-kappaB) p65 activation.
Positive_regulation (activation) of Protein_catabolism (degradation) of IkBalpha
1) Confidence 0.46 Published 2002 Journal J. Neuroimmunol. Section Abstract Doc Link 12417429 Disease Relevance 0.33 Pain Relevance 0.29
Investigating the molecular mechanisms by which parthenolide prevents iNOS/NO synthesis, we found that parthenolide inhibits the activation of p42/44 mitogen-activated protein kinase (MAPK), but not IkBalpha (IkappaBalpha) degradation or nuclear factor-kappaB (NF-kappaB) p65 activation.
Neg (not) Positive_regulation (activation) of Protein_catabolism (degradation) of IkBalpha
2) Confidence 0.46 Published 2002 Journal J. Neuroimmunol. Section Abstract Doc Link 12417429 Disease Relevance 0.32 Pain Relevance 0.29
Investigating the molecular mechanisms by which parthenolide prevents iNOS/NO synthesis, we found that parthenolide inhibits the activation of p42/44 mitogen-activated protein kinase (MAPK), but not IkBalpha (IkappaBalpha) degradation or nuclear factor-kappaB (NF-kappaB) p65 activation.
Neg (not) Positive_regulation (activation) of Protein_catabolism (degradation) of IkappaBalpha
3) Confidence 0.40 Published 2002 Journal J. Neuroimmunol. Section Abstract Doc Link 12417429 Disease Relevance 0.32 Pain Relevance 0.29
Investigating the molecular mechanisms by which parthenolide prevents iNOS/NO synthesis, we found that parthenolide inhibits the activation of p42/44 mitogen-activated protein kinase (MAPK), but not IkBalpha (IkappaBalpha) degradation or nuclear factor-kappaB (NF-kappaB) p65 activation.
Positive_regulation (activation) of Protein_catabolism (degradation) of IkappaBalpha
4) Confidence 0.40 Published 2002 Journal J. Neuroimmunol. Section Abstract Doc Link 12417429 Disease Relevance 0.33 Pain Relevance 0.29
Diclofenac induced the degradation of IkappaBalpha, which increased free nuclear factor kappaB (NF-kappaB) in cells.
Positive_regulation (induced) of Protein_catabolism (degradation) of IkappaBalpha associated with diclofenac
5) Confidence 0.08 Published 2005 Journal FEBS Lett. Section Abstract Doc Link 16051228 Disease Relevance 0.34 Pain Relevance 0.45
The transcription factor nuclear factor-kappaB (NF-kappaB) is constitutively activated in malignancies from enhanced activity of inhibitor of NF-kappaB (IkappaB) kinase, with accelerated IkappaBalpha degradation.
Positive_regulation (accelerated) of Protein_catabolism (degradation) of IkappaBalpha
6) Confidence 0.07 Published 2001 Journal Am. J. Physiol., Cell Physiol. Section Abstract Doc Link 11171586 Disease Relevance 0.30 Pain Relevance 0.08
IkappaBalpha degradation, NF-kappaB activation, and iNOS expression were attenuated by parthenolide (3mg/kg), the active constituent of feverfew, an anti-inflammatory drug used for migraine treatment.
Positive_regulation (activation) of Protein_catabolism (degradation) of IkappaBalpha associated with inflammation and migraine
7) Confidence 0.06 Published 2002 Journal Ann. Neurol. Section Abstract Doc Link 11921057 Disease Relevance 0.70 Pain Relevance 0.57
The transcription factor nuclear factor-kappaB (NF-kappaB) is constitutively activated in malignancies from enhanced activity of inhibitor of NF-kappaB (IkappaB) kinase, with accelerated IkappaBalpha degradation.
Positive_regulation (activated) of Protein_catabolism (degradation) of IkappaBalpha
8) Confidence 0.05 Published 2001 Journal Am. J. Physiol., Cell Physiol. Section Abstract Doc Link 11171586 Disease Relevance 0.30 Pain Relevance 0.08
Consistently gamma-mangostin was also observed to decrease the LPS-induced IkappaB degradation and phosphorylation in a concentration-dependent manner, as assayed by immunoblotting.
Positive_regulation (-) of Protein_catabolism (degradation) of IkappaB
9) Confidence 0.01 Published 2004 Journal Mol. Pharmacol. Section Abstract Doc Link 15322259 Disease Relevance 0.20 Pain Relevance 0.06
Because LPS is known to stimulate inhibitor kappaB (IkappaB) kinase (IKK)-mediated phosphorylation of IkappaB followed by its degradation, which in turn induces nuclear factor (NF)-kappaB nuclear translocation leading to transcriptional activation of COX-2 gene, the effect of gamma-mangostin on the IKK/IkappaB cascade controlling the NF-kappaB activation was examined.
Spec (examined) Positive_regulation (stimulate) of Protein_catabolism (degradation) of IkappaB
10) Confidence 0.01 Published 2004 Journal Mol. Pharmacol. Section Abstract Doc Link 15322259 Disease Relevance 0.15 Pain Relevance 0
Consistently gamma-mangostin was also observed to decrease the LPS-induced IkappaB degradation and phosphorylation in a concentration-dependent manner, as assayed by immunoblotting.
Positive_regulation (induced) of Protein_catabolism (degradation) of IkappaB
11) Confidence 0.01 Published 2004 Journal Mol. Pharmacol. Section Abstract Doc Link 15322259 Disease Relevance 0.20 Pain Relevance 0.06
Furthermore, unlike aspirin, SC236 affected neither the phosphorylation, degradation, nor expression of IkappaB-alpha, suggesting that the effects of SC236 are independent of IKK activity and IkappaB-alpha gene transcription.
Neg (neither) Positive_regulation (affected) of Protein_catabolism (degradation) of IkappaB-alpha associated with aspirin
12) Confidence 0.00 Published 2003 Journal Oncogene Section Abstract Doc Link 12606945 Disease Relevance 0.38 Pain Relevance 0.26

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