INT106524

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Context Info
Confidence 0.80
First Reported 2003
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 23
Total Number 24
Disease Relevance 15.35
Pain Relevance 4.78

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) nucleus (Jun) DNA binding (Jun)
transcription factor binding (Jun)
Anatomy Link Frequency
liver 1
T cells 1
hippocampus 1
Jun (Mus musculus)
Pain Link Frequency Relevance Heat
Hippocampus 12 98.24 Very High Very High Very High
Paracetamol 43 97.44 Very High Very High Very High
tolerance 19 96.52 Very High Very High Very High
Eae 1 94.92 High High
diclofenac 12 94.80 High High
Spinal cord 3 92.48 High High
cytokine 262 90.84 High High
Inflammation 380 90.44 High High
COX-2 inhibitor 3 88.16 High High
alcohol 33 82.88 Quite High
Disease Link Frequency Relevance Heat
Stress 192 99.62 Very High Very High Very High
Neurodegenerative Disease 32 99.28 Very High Very High Very High
Apoptosis 299 99.12 Very High Very High Very High
Injury 29 98.16 Very High Very High Very High
Obesity 162 96.36 Very High Very High Very High
Toxicity 37 95.68 Very High Very High Very High
Reprotox - General 1 48 93.60 High High
Necrosis 13 92.64 High High
Frailty 2 92.48 High High
Cancer 287 92.28 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Phosphorylation of c-Jun NH(2)-terminal kinase (JNK) was analyzed by Western blotting.
Spec (analyzed) Phosphorylation (Phosphorylation) of c-Jun
1) Confidence 0.80 Published 2010 Journal Am. J. Physiol. Gastrointest. Liver Physiol. Section Abstract Doc Link 20539006 Disease Relevance 1.05 Pain Relevance 0.46
In JB6, Cox-2(-/-), or wild-type Cox-2(+/+) cells, both NS-398 and piroxicam inhibited UVB-induced phosphorylation of c-Jun NH(2)-terminal kinases, the kinases that activate the AP-1/c-Jun complex.
Phosphorylation (phosphorylation) of c-Jun
2) Confidence 0.60 Published 2003 Journal J. Biol. Chem. Section Abstract Doc Link 12433932 Disease Relevance 0.14 Pain Relevance 0.19
Furthermore, APAP treatment significantly upregulated jun oncogene (c-Jun) gene expression, which was confirmed by Western blotting for both the phosphorylated and the nonphosphorylated forms of c-Jun protein.
Phosphorylation (phosphorylated) of c-Jun associated with paracetamol
3) Confidence 0.53 Published 2010 Journal Toxicol. Sci. Section Abstract Doc Link 20363829 Disease Relevance 0.36 Pain Relevance 0.87
Furthermore, APAP treatment significantly upregulated jun oncogene (c-Jun) gene expression, which was confirmed by Western blotting for both the phosphorylated and the nonphosphorylated forms of c-Jun protein.
Phosphorylation (nonphosphorylated) of c-Jun associated with paracetamol
4) Confidence 0.53 Published 2010 Journal Toxicol. Sci. Section Abstract Doc Link 20363829 Disease Relevance 0.36 Pain Relevance 0.86
The most well known substrate for JNK is c-jun and JNK activation is synonymous with c-jun phosphorylation.
Phosphorylation (phosphorylation) of jun
5) Confidence 0.52 Published 2004 Journal Cell Commun Signal Section Body Doc Link PMC449737 Disease Relevance 0.37 Pain Relevance 0
Activated JNKs phosphorylate c-Jun, JunD, ATF, and other transcriptional factors, which are involved in the formation and activation of the AP-1 complex [43].
Phosphorylation (phosphorylate) of Jun
6) Confidence 0.49 Published 2010 Journal Gastroenterology Research and Practice Section Body Doc Link PMC2995932 Disease Relevance 0.78 Pain Relevance 0.06
and c-Jun (a phosphorylation target of ERK and JNK).
Phosphorylation (phosphorylation) of c-Jun
7) Confidence 0.47 Published 2004 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC1082887 Disease Relevance 0.18 Pain Relevance 0
In addition, mutating the activating phosphorylation sites on c-jun protects against neuronal apoptosis in the hippocampus [122].
Phosphorylation (phosphorylation) of c-jun in hippocampus associated with hippocampus and neurodegenerative disease
8) Confidence 0.37 Published 2010 Journal PPAR Research Section Body Doc Link PMC2748193 Disease Relevance 0.88 Pain Relevance 0.24
JNK phosphorylation, c-jun gene expression, and caspase-3
Phosphorylation (phosphorylation) of c-jun
9) Confidence 0.36 Published 2004 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC1082887 Disease Relevance 0.79 Pain Relevance 0.03
This analysis revealed, that basal JNK activity, as assessed by phosphorylation of c-Jun, was significantly reduced in skeletal muscle and exhibited a trend towards reduction in liver of obese IR?
Phosphorylation (phosphorylation) of c-Jun in liver associated with obesity
10) Confidence 0.36 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2865520 Disease Relevance 0.92 Pain Relevance 0.25
Immunoblot studies with a phosphospecific JNK antibody revealed that JNK1/2 (p46) was activated at 6 h, leading to phosphorylation of the downstream target c-Jun.
Phosphorylation (phosphorylation) of c-Jun
11) Confidence 0.36 Published 2009 Journal Am. J. Physiol. Gastrointest. Liver Physiol. Section Abstract Doc Link 20501447 Disease Relevance 0.86 Pain Relevance 0.73
Dwarf mice exhibited lower responses in the MEK-ERK kinase cascade and a lack of c-Jun Ser63 phosphorylation, suggesting altered management of oxidative stress in the long-lived dwarfs compared with the wild-type control mice.
Phosphorylation (phosphorylation) of c-Jun associated with stress
12) Confidence 0.33 Published 2006 Journal Age (Dordr) Section Body Doc Link PMC2464727 Disease Relevance 0.58 Pain Relevance 0
Acetaldehyde is known to trigger both oxidative stress and apoptosis via activation of stress signaling such as c-Jun phosphorylation [5], [24], [25].
Phosphorylation (phosphorylation) of c-Jun associated with stress and apoptosis
13) Confidence 0.32 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2807457 Disease Relevance 1.11 Pain Relevance 0.07
The expression levels of phosphorylated c-Jun N-Terminal Kinase (pJNK) were next examined using whole cell lysate.
Phosphorylation (phosphorylated) of Jun
14) Confidence 0.28 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2668769 Disease Relevance 0.61 Pain Relevance 0.09
Ethanol or acetaldehyde has been shown to trigger oxidative stress and apoptosis via activation of stress signaling such as c-Jun phosphorylation [1]–[3].
Phosphorylation (phosphorylation) of c-Jun associated with stress and apoptosis
15) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2890411 Disease Relevance 0.39 Pain Relevance 0.04
It also contains a variety of transcription factor binding sites, including those for Sp1, GATA-1, AP1, AP2, CREB, estrogen and glucocorticoid receptors, NF?
Phosphorylation (those) of AP1
16) Confidence 0.20 Published 2007 Journal Current Genomics Section Body Doc Link PMC2647160 Disease Relevance 0.55 Pain Relevance 0
PTPH1 overexpression in Jurkat T cells reduces indirectly the TCR-induced serine phosphorylation of Mek, Erk, Jnk and AP-1 leading to a decreased IL-2 gene activation [13].
Phosphorylation (phosphorylation) of AP-1 in T cells
17) Confidence 0.19 Published 2010 Journal J Inflamm (Lond) Section Body Doc Link PMC2873500 Disease Relevance 0.22 Pain Relevance 0.04
Only specific blocking of p-JNK significantly inhibited the induction of apoptosis by chemotherapy (Figure 5b), whereas the level of phosphorylated c-Jun as the target of activated JNK was effectively decreased by the JNK inhibitor SP600125 (Fig. 5c).


Phosphorylation (phosphorylated) of c-Jun associated with apoptosis
18) Confidence 0.18 Published 2006 Journal J Carcinog Section Body Doc Link PMC1665446 Disease Relevance 1.02 Pain Relevance 0
While treatment of KNS62 with either GEM or PB induces phosphorylation of ERK1/2, p38, JNK and its target c-Jun, combination therapy amplifies this effect substantially (Figure 5a).
Phosphorylation (phosphorylation) of c-Jun
19) Confidence 0.14 Published 2006 Journal J Carcinog Section Body Doc Link PMC1665446 Disease Relevance 0.67 Pain Relevance 0
Additionally, ST2L is able to activate the transcription factor AP-1; increase phosphorylation of c-Jun, and activate the MAP kinases c-Jun N-terminal kinase (JNK), p42/p44 and p38.
Phosphorylation (phosphorylation) of c-Jun
20) Confidence 0.12 Published 2008 Journal J Occup Med Toxicol Section Body Doc Link PMC2259400 Disease Relevance 0.14 Pain Relevance 0.12

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