INT101722

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Context Info
Confidence 0.31
First Reported 2002
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 12
Total Number 13
Disease Relevance 2.21
Pain Relevance 0.73

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

nucleus (JUND)
Anatomy Link Frequency
epithelial cells 2
chondrocytes 1
JUND (Homo sapiens)
Pain Link Frequency Relevance Heat
cINOD 2 96.12 Very High Very High Very High
cytokine 42 93.96 High High
qutenza 3 92.72 High High
opioid receptor 6 82.76 Quite High
Bioavailability 1 79.12 Quite High
dexamethasone 4 71.80 Quite High
Kinase C 2 63.44 Quite High
Osteoarthritis 137 52.08 Quite High
cocaine 1 48.52 Quite Low
Inflammation 47 44.40 Quite Low
Disease Link Frequency Relevance Heat
Occupational Lung Diseases 10 99.64 Very High Very High Very High
Apoptosis 141 98.24 Very High Very High Very High
Asthma 122 92.16 High High
Repression 10 91.84 High High
Cancer 19 76.72 Quite High
Neuroblastoma 1 75.56 Quite High
Osteoarthritis 138 52.08 Quite High
INFLAMMATION 49 44.40 Quite Low
Necrosis 10 8.36 Low Low
Disease 22 7.84 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Some of these agents (EGCG, genistein, and curcumin) appear to directly target specific RTKs, and all of these compounds cause inhibition of the activity of the transcription factors AP-1 and NF-kappaB, thus inhibiting cell proliferation and enhancing apoptosis.
AP-1 Binding (activity) of associated with apoptosis
1) Confidence 0.31 Published 2005 Journal Mutat. Res. Section Abstract Doc Link 15992833 Disease Relevance 0.39 Pain Relevance 0.13
AP-1 binding assay
AP-1 Binding (assay) of
2) Confidence 0.27 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212570 Disease Relevance 0 Pain Relevance 0
AP-1 binding assay
AP-1 Binding (binding) of
3) Confidence 0.27 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212570 Disease Relevance 0 Pain Relevance 0
AP-1 consensus nucleotide binding activity from nuclear extracts (8 ?
AP-1 Binding (binding) of
4) Confidence 0.27 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212570 Disease Relevance 0 Pain Relevance 0
MMP expression is regulated by transcription factors such as the AP-1 complex, which is activated by phosphorylated MAPKs.
AP-1 Binding (complex) of
5) Confidence 0.27 Published 2007 Journal Arthritis Res Ther Section Abstract Doc Link PMC2212570 Disease Relevance 0 Pain Relevance 0
AP-1 transcription factor activation was evaluated by measuring AP-1 DNA-binding activity.
AP-1 Binding (activity) of
6) Confidence 0.26 Published 2007 Journal Arthritis Res Ther Section Abstract Doc Link PMC2212570 Disease Relevance 0 Pain Relevance 0
AP-1 transcription factor activation was evaluated by measuring AP-1 DNA-binding activity.
AP-1 Binding (binding) of
7) Confidence 0.26 Published 2007 Journal Arthritis Res Ther Section Abstract Doc Link PMC2212570 Disease Relevance 0 Pain Relevance 0
AP-1 binding to these elements was confirmed using electrophoretic mobility shift and immunoshift assays.
AP-1 Binding (binding) of
8) Confidence 0.23 Published 2002 Journal Mol. Pharmacol. Section Abstract Doc Link 11901219 Disease Relevance 0.08 Pain Relevance 0.24
JNK increases the expression of JunD, and JunD acts with NF-?
JunD Binding (acts) of
9) Confidence 0.17 Published 2010 Journal BMC Genomics Section Body Doc Link PMC2996966 Disease Relevance 0.27 Pain Relevance 0
Studies have shown that the glucocorticoid receptor (GR) in GCR asthmatics exhibits a lower interaction with activator protein-1 (AP-1), and this effect is accompanied by raised levels of AP-1.[26] Mathieu et al. have shown that overexpression of the GR gene in A549 human lung epithelial cells, using a GR expression vector, resulted in repression of both nuclear factor kappa-B (NF-?
AP-1 Binding (interaction) of in epithelial cells associated with repression and occupational lung diseases
10) Confidence 0.10 Published 2010 Journal Indian Journal of Human Genetics Section Body Doc Link PMC3009420 Disease Relevance 0.71 Pain Relevance 0.12
Studies have shown that the glucocorticoid receptor (GR) in GCR asthmatics exhibits a lower interaction with activator protein-1 (AP-1), and this effect is accompanied by raised levels of AP-1.[26] Mathieu et al. have shown that overexpression of the GR gene in A549 human lung epithelial cells, using a GR expression vector, resulted in repression of both nuclear factor kappa-B (NF-?
activator protein-1 Binding (interaction) of in epithelial cells associated with repression and occupational lung diseases
11) Confidence 0.10 Published 2010 Journal Indian Journal of Human Genetics Section Body Doc Link PMC3009420 Disease Relevance 0.71 Pain Relevance 0.12
B pathways in chondrocytes has been shown to cause activation of their downstream transcription factors, including activation protein-1 (AP-1) and NF-?
AP-1 Binding (factors) of in chondrocytes
12) Confidence 0.03 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2656251 Disease Relevance 0.05 Pain Relevance 0.03
Binding of activator protein-1 (AP-1) to the 12-tetradecanoylphorbol-13-acetate-responsive element (TRE) sequence in LPS-stimulated cells was inhibited by bis-FA at 1 microM and dehydrodiisoeugenol at 0.1 microM, but not by the parent monomers isoeugenol and ferulic acid.
AP-1 Binding (Binding) of
13) Confidence 0.01 Published 2005 Journal In Vivo Section Abstract Doc Link 16277019 Disease Relevance 0 Pain Relevance 0.10

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