INT17331

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Context Info
Confidence 0.69
First Reported 1991
Last Reported 2010
Negated 3
Speculated 7
Reported most in Abstract
Documents 132
Total Number 139
Disease Relevance 60.40
Pain Relevance 27.03

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) nucleoplasm (JUN) nuclear chromosome (JUN)
aging (JUN) nucleus (JUN) DNA binding (JUN)
Anatomy Link Frequency
skin 4
T lymphocytes 3
macrophages 2
chondrocytes 2
HL-60 2
JUN (Homo sapiens)
Pain Link Frequency Relevance Heat
cINOD 106 99.98 Very High Very High Very High
opioid receptor 26 99.90 Very High Very High Very High
Inflammatory stimuli 11 99.84 Very High Very High Very High
Kappa opioid receptor 13 99.82 Very High Very High Very High
qutenza 64 99.78 Very High Very High Very High
metalloproteinase 642 99.66 Very High Very High Very High
Enkephalin 18 99.64 Very High Very High Very High
lidocaine 10 99.62 Very High Very High Very High
cytokine 327 99.58 Very High Very High Very High
aspirin 65 99.48 Very High Very High Very High
Disease Link Frequency Relevance Heat
Stress 300 100.00 Very High Very High Very High
Apoptosis 2568 99.90 Very High Very High Very High
Skin Cancer 55 99.90 Very High Very High Very High
INFLAMMATION 687 99.84 Very High Very High Very High
Glioma 8 99.80 Very High Very High Very High
Adhesions 36 99.78 Very High Very High Very High
Infection 534 99.76 Very High Very High Very High
Colon Cancer 110 99.72 Very High Very High Very High
Glioblastoma 4 99.68 Very High Very High Very High
Cancer 871 99.64 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
After 1 h or 96 h of treatment, Fos and Jun protein levels were altered and the DNA-binding activity of AP-1 was increased in response to both substances.
Positive_regulation (increased) of AP-1
1) Confidence 0.69 Published 2005 Journal Neuropharmacology Section Abstract Doc Link 15814102 Disease Relevance 0.08 Pain Relevance 0.35
RESULTS: Sevoflurane inhibited activation of the transcription factor AP-1.
Positive_regulation (activation) of AP-1
2) Confidence 0.69 Published 2004 Journal Anesthesiology Section Body Doc Link 15329596 Disease Relevance 0 Pain Relevance 0
Additional work by Hideshima et al revealed that bortezomib activation seemed to be dependent on the activation of c-Jun NH2-terminal kinase (JNK) and subsequently caspases-8 and caspase-3 that elicit DNA damage and apoptosis.
Positive_regulation (activation) of c-Jun associated with apoptosis
3) Confidence 0.67 Published 2010 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2990320 Disease Relevance 0.48 Pain Relevance 0.04
However, pBrBzGSCp(2) did not lead to tau "hyper"-phosphorylation despite activation of p38 mitogen-activated protein kinase and c-Jun NH(2)-terminal kinase but rather activated protein phosphatases 2 and induced tau dephosphorylation at the Ser(202)/Thr(205) and Ser(396)/Ser(404) epitopes.
Positive_regulation (activation) of c-Jun
4) Confidence 0.67 Published 2006 Journal J. Neurosci. Res. Section Abstract Doc Link 16555297 Disease Relevance 0.61 Pain Relevance 0.09
Transforming growth factor-activated kinase 1 (TAK1), a member of the MAPK kinase kinase family, is indispensable for the activation of c-Jun N-terminal kinase (JNK) and p38 MAPK.
Positive_regulation (activation) of c-Jun
5) Confidence 0.67 Published 2008 Journal Glia Section Abstract Doc Link 18293403 Disease Relevance 0.63 Pain Relevance 0.26
RESULTS: SC236 treatment induced apoptosis in gastric cancer cells and caused activation of p38 and stress-activated protein kinase/jun kinase, but down-regulated Akt/PKB.
Positive_regulation (activation) of jun
6) Confidence 0.67 Published 2006 Journal Digestion Section Body Doc Link 16641552 Disease Relevance 0.16 Pain Relevance 0
Analysis of MAP kinase activity revealed a transient activation of c-Jun N-terminal kinase (JNK) and p38 after LPS stimulation.
Positive_regulation (activation) of c-Jun
7) Confidence 0.67 Published 2002 Journal J. Immunol. Section Abstract Doc Link 12444149 Disease Relevance 0.05 Pain Relevance 0.13
METHODS: The authors used primary sensory neuron cultures and pheochromocytoma cell line cultures to detect time-dependent activation of the p38 MAPK or related pathways such as extracellular signal-regulated kinases and c-jun N-terminal kinases.
Positive_regulation (activation) of c-jun in primary sensory neuron
8) Confidence 0.67 Published 2006 Journal Anesthesiology Section Body Doc Link 17065898 Disease Relevance 0 Pain Relevance 0
RESULTS: All types of dorsal root ganglion cells were subject to neurotoxic effects of lidocaine, which were mediated by specific activation of the p38 MAPK but not extracellular signal-regulated kinases or c-jun N-terminal kinases.
Positive_regulation (activation) of c-jun in dorsal root ganglion
9) Confidence 0.67 Published 2006 Journal Anesthesiology Section Body Doc Link 17065898 Disease Relevance 0 Pain Relevance 0
Phosphatidylinositol-3 kinase is distinctively required for mu-, but not kappa-opioid receptor-induced activation of c-Jun N-terminal kinase.
Positive_regulation (activation) of c-Jun associated with kappa opioid receptor
10) Confidence 0.67 Published 2004 Journal J. Neurochem. Section Title Doc Link 15056283 Disease Relevance 0.08 Pain Relevance 0.47
In this study, we investigated the effects of morphine and nitric oxide on CD14 expression and activator protein 1 activation in human blood monocytes and neutrophils as well as the leukocyte cell line HL-60.
Spec (investigated) Positive_regulation (activation) of activator protein 1 in monocytes associated with morphine
11) Confidence 0.61 Published 2007 Journal Eur J Anaesthesiol Section Abstract Doc Link 17583593 Disease Relevance 0 Pain Relevance 0.21
Aspirin and aspirin-like salicylates inhibited the activation of AP-1 in the same dose range as seen for the inhibition of tumor promoter-induced transformation.
Positive_regulation (activation) of AP-1 associated with aspirin and cancer
12) Confidence 0.57 Published 1997 Journal J. Biol. Chem. Section Abstract Doc Link 9092536 Disease Relevance 0.77 Pain Relevance 0.43
In addition, PKC and AP1 subunits c-Jun and c-Fos were also upregulated.
Positive_regulation (upregulated) of c-Jun
13) Confidence 0.56 Published 2001 Journal Anticancer Res. Section Body Doc Link 11501838 Disease Relevance 0.07 Pain Relevance 0
In addition, PKC and AP1 subunits c-Jun and c-Fos were also upregulated.
Positive_regulation (upregulated) of AP1
14) Confidence 0.56 Published 2001 Journal Anticancer Res. Section Body Doc Link 11501838 Disease Relevance 0.07 Pain Relevance 0
After binding of its ligand the tumor GnRH receptor couples to G-protein alphai and activates a variety of intracellular signaling mechanisms. (1) Through activation of a protein tyrosine phosphatase, autophosphorylation of growth factor receptors is reverted leading to an inhibition of mitogenic signaling and reduced cell proliferation. (2) Through activation of nuclear factor kappa B antiapoptotic mechanisms are induced protecting tumor cells from apoptosis induced, for example, by doxorubicin. (3) Through activation of the Jun kinase pathway AP-1 is induced, leading to cell cycle arrest in the G0/G1 phase.
Positive_regulation (activation) of Jun associated with cancer and apoptosis
15) Confidence 0.53 Published 2003 Journal Endocr. Relat. Cancer Section Abstract Doc Link 12790790 Disease Relevance 0.80 Pain Relevance 0.18
After binding of its ligand the tumor GnRH receptor couples to G-protein alphai and activates a variety of intracellular signaling mechanisms. (1) Through activation of a protein tyrosine phosphatase, autophosphorylation of growth factor receptors is reverted leading to an inhibition of mitogenic signaling and reduced cell proliferation. (2) Through activation of nuclear factor kappa B antiapoptotic mechanisms are induced protecting tumor cells from apoptosis induced, for example, by doxorubicin. (3) Through activation of the Jun kinase pathway AP-1 is induced, leading to cell cycle arrest in the G0/G1 phase.
Positive_regulation (activation) of AP-1 associated with cancer and apoptosis
16) Confidence 0.53 Published 2003 Journal Endocr. Relat. Cancer Section Abstract Doc Link 12790790 Disease Relevance 0.81 Pain Relevance 0.18
We concluded that, in herniated disc tissue, the oncoproteins c-Fos and c-Jun are activated in disc cells and cell clusters.
Positive_regulation (activated) of c-Jun associated with intervertebral disk displacement
17) Confidence 0.50 Published 2002 Journal Eur Spine J Section Abstract Doc Link 12384753 Disease Relevance 0.33 Pain Relevance 0.10
The oncoproteins c-Fos and c-Jun create a transcriptional site early response activating protein (AP-1) mediating the regulation of gene expression in response to extracellular signalling by, for example, cytokines.
Positive_regulation (mediating) of AP-1 associated with cytokine
18) Confidence 0.50 Published 2002 Journal Eur Spine J Section Abstract Doc Link 12384753 Disease Relevance 0.07 Pain Relevance 0.05
Moreover the induction of metalloproteinase gene appears to utilise the c-jun oncogene as intracellular messenger.
Spec (appears) Positive_regulation (utilise) of c-jun associated with metalloproteinase
19) Confidence 0.50 Published 1999 Journal Anticancer Res. Section Abstract Doc Link 10216507 Disease Relevance 0.50 Pain Relevance 0.15
In conclusion; a) in pancreatic cancer, the expression of c-jun is increased in tumour cells in majority of cases as compared to the control group, b) a c-jun positivity is also found in alpha cells with a pattern not different from control group, but the relation between the alpha cells and c-jun production is unknown, c) c-jun expression does not vary in relation to histological findings.
Positive_regulation (found) of c-jun in alpha cells associated with cancer and pancreatic cancer
20) Confidence 0.50 Published 1999 Journal Anticancer Res. Section Abstract Doc Link 10216507 Disease Relevance 0.73 Pain Relevance 0.24

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