INT75133

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Context Info
Confidence 0.51
First Reported 1998
Last Reported 2010
Negated 3
Speculated 1
Reported most in Abstract
Documents 15
Total Number 16
Disease Relevance 6.69
Pain Relevance 3.26

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
HL-60 1
pores 1
HGF 1
JUND (Homo sapiens)
Pain Link Frequency Relevance Heat
endometriosis 108 99.84 Very High Very High Very High
Kinase C 4 99.56 Very High Very High Very High
metalloproteinase 3 99.04 Very High Very High Very High
qutenza 15 98.90 Very High Very High Very High
opioid receptor 12 98.40 Very High Very High Very High
Osteoarthritis 45 95.44 Very High Very High Very High
Inflammation 27 94.16 High High
aspirin 7 93.04 High High
dexamethasone 2 91.08 High High
cocaine 2 89.32 High High
Disease Link Frequency Relevance Heat
Stress 15 100.00 Very High Very High Very High
Endometriosis 138 99.84 Very High Very High Very High
Apoptosis 89 99.78 Very High Very High Very High
Repression 3 99.12 Very High Very High Very High
Cancer 34 98.64 Very High Very High Very High
Skin Cancer 2 95.80 Very High Very High Very High
Neuroblastoma 2 95.72 Very High Very High Very High
Osteoarthritis 45 95.44 Very High Very High Very High
Obesity 2 95.12 Very High Very High Very High
INFLAMMATION 28 94.16 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Nevertheless, 2.5 mmol/l was almost as 10 mmol/l glucosamine in terms of affect on MAPK phosphorylation and AP-1 activation.
Positive_regulation (activation) of AP-1
1) Confidence 0.51 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212570 Disease Relevance 0.08 Pain Relevance 0.04
It achieved this by affecting phosphorylation of JNK and p38 MAPKs and consequently inhibiting c-jun and junD activation.
Positive_regulation (activation) of junD
2) Confidence 0.34 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2212570 Disease Relevance 0.24 Pain Relevance 0.12
AP-1 transcription factor activation was evaluated by measuring AP-1 DNA-binding activity.
Positive_regulation (activation) of AP-1
3) Confidence 0.34 Published 2007 Journal Arthritis Res Ther Section Abstract Doc Link PMC2212570 Disease Relevance 0 Pain Relevance 0
In this report, we show that TPA activates AP-1 as well as the transcription factor nuclear factor kappaB (NFkappaB) in the mu-opioid receptor expressing neuroblastoma cell line SH SY5Y.
Positive_regulation (activates) of AP-1 associated with neuroblastoma and opioid receptor
4) Confidence 0.24 Published 2002 Journal Mol. Pharmacol. Section Abstract Doc Link 11901219 Disease Relevance 0.10 Pain Relevance 0.59
In addition, transcription of the mu-opioid receptor gene is induced by the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), an activator of protein kinase C, which in turn is an activator of AP-1 transcription factors.
Positive_regulation (activator) of AP-1 associated with kinase c and opioid receptor
5) Confidence 0.23 Published 2002 Journal Mol. Pharmacol. Section Abstract Doc Link 11901219 Disease Relevance 0.07 Pain Relevance 0.62
In contrast, after the prolonged exposure of 6 h, three transcription regulators involved in lipid/fatty acid metabolism and protection from oxidative stress as a result of this metabolism (JUND, GTF21 and TSC22-D1) were upregulated in comparison to the placebo treatment (Figure 2).
Positive_regulation (result) of JUND associated with stress
6) Confidence 0.19 Published 2008 Journal BMC Genomics Section Body Doc Link PMC2519092 Disease Relevance 0.33 Pain Relevance 0
After 6 h exposure, the transcription regulators JUND, GTF2I and TSC22-D1, which are involved in protection from oxidative stress and lipid/fatty acid metabolism, GPX4, which is involved in protection against oxidative stress, the fatty acid binding protein FABP1, the thrombospondin receptor (or fatty acid translocase) CD36, six acyl-CoA genes and isocitrate dehydrogenase-1 (IDH1), which is one of the more "central" hub proteins were all upregulated.
Positive_regulation (upregulated) of JUND associated with stress
7) Confidence 0.14 Published 2008 Journal BMC Genomics Section Body Doc Link PMC2519092 Disease Relevance 0.38 Pain Relevance 0
This is in contrast to other studies carried out in different cells, which have shown GR-mediated AP-1 and NF-?
Positive_regulation (mediated) of AP-1
8) Confidence 0.13 Published 2010 Journal Indian Journal of Human Genetics Section Body Doc Link PMC3009420 Disease Relevance 0.61 Pain Relevance 0.11
Furthermore, the proto-oncogenes AXL, SHC1, and JUND are elevated in endometriosis (Table 2).
Positive_regulation (elevated) of JUND associated with endometriosis
9) Confidence 0.12 Published 2008 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2615013 Disease Relevance 0.89 Pain Relevance 0.38
We suggest that ROS generation by inhibition of the NADH-dependent plasma membrane electron transport system resulted in the oxidation of mitochondrial megachannel pores that allows for the disruption of deltapsi(m) and apoptosis, and that AP-1 activation is not required for vanilloid-induced apoptosis.
Positive_regulation (activation) of AP-1 in pores associated with apoptosis
10) Confidence 0.07 Published 1998 Journal Cell Growth Differ. Section Abstract Doc Link 9580328 Disease Relevance 0.40 Pain Relevance 0.07
Despite the activation of JNK, there was no induction of activator protein 1 (AP-1) activity as determined by gel shift assay or of induction of an AP-1-responsive reporter.
Spec (determined) Positive_regulation (induction) of AP-1
11) Confidence 0.07 Published 1998 Journal Cell Growth Differ. Section Abstract Doc Link 9580328 Disease Relevance 0.35 Pain Relevance 0.14
Despite the activation of JNK, there was no induction of activator protein 1 (AP-1) activity as determined by gel shift assay or of induction of an AP-1-responsive reporter.
Neg (no) Positive_regulation (induction) of AP-1
12) Confidence 0.07 Published 1998 Journal Cell Growth Differ. Section Abstract Doc Link 9580328 Disease Relevance 0.37 Pain Relevance 0.15
Induction of apoptosis by vanilloid compounds does not require de novo gene transcription and activator protein 1 activity.
Neg (not) Positive_regulation (require) of activator protein 1 associated with qutenza and apoptosis
13) Confidence 0.07 Published 1998 Journal Cell Growth Differ. Section Title Doc Link 9580328 Disease Relevance 0.43 Pain Relevance 0.26
Despite the activation of JNK, there was no induction of activator protein 1 (AP-1) activity as determined by gel shift assay or of induction of an AP-1-responsive reporter.
Neg (no) Positive_regulation (induction) of activator protein 1
14) Confidence 0.07 Published 1998 Journal Cell Growth Differ. Section Abstract Doc Link 9580328 Disease Relevance 0.37 Pain Relevance 0.15
However, both agents inhibited the kinase activity of ERK1/2 induced by HGF and repressed HGF-induced phosphorylation of 90-kd ribosomal S6 kinase (RSK) and Elk-1, key downstream substrates of ERK1/2, resulting in the suppression of transcriptional activity of Elk-1 as well as nuclear factor kappaB (NF-kappaB) and AP-1, which are involved in MMP-9 gene regulation.
Positive_regulation (resulting) of AP-1 in HGF associated with metalloproteinase
15) Confidence 0.03 Published 2002 Journal Hepatology Section Abstract Doc Link 11981761 Disease Relevance 0.39 Pain Relevance 0.46
For instance, [6]-gingerol inhibited pulmonary metastasis in mice bearing B16F10 melanoma cells through the activation of CD8+ T cells.8 It also inhibited tumor promotion of ICR mice induced skin tumor by tumor promoter (TPA),9 and blocked the azoxymethane-induced intestinal carcinogenesis in rodents.10 [6]-Gingerol interfered with EGF-induced transformation of mouse epidermal JB6 cell line, and reduced the activation of Activator Protein-1 (AP-1), which plays a critical role in tumor promotion.11 Moreover, [6]-gingerol exerted inhibitory effects on the cell viability and DNA synthesis, also induced apoptosis of human promyelocytic leukemia HL-60 cells.12 Recently, it has been reported that ginger root extracts and gingerol inhibit the growth of Helicobacter pylori CagA+ strains, which has a specific gene linked to the development of gastric premalignant and malignant lesions.13 It suggests that ginger and gingerol have effects of chemoprevention to the gastric-intestinal cancers.
Positive_regulation (activation) of AP-1 in HL-60 associated with leukemia, ulcers, intestinal cancer, apoptosis, skin cancer, metastasis, malignant neoplastic disease, cancer and sprains and strains
16) Confidence 0.01 Published 2006 Journal Yonsei Medical Journal Section Body Doc Link PMC2687755 Disease Relevance 1.69 Pain Relevance 0.16

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