INT96063

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.67
First Reported 2001
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 9
Disease Relevance 4.06
Pain Relevance 1.38

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) aging (Jun) nucleus (Jun)
DNA binding (Jun) transcription factor binding (Jun)
Anatomy Link Frequency
sciatic nerves 2
neurons 2
Jun (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Inflammation 128 100.00 Very High Very High Very High
Inflammatory response 12 98.50 Very High Very High Very High
Sciatic nerve 23 98.44 Very High Very High Very High
Neuritis 8 96.12 Very High Very High Very High
cytokine 68 94.00 High High
dexamethasone 2 93.04 High High
Inflammatory mediators 20 37.40 Quite Low
Enkephalin 2 25.00 Low Low
metalloproteinase 29 5.84 Low Low
Spinal cord 22 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 157 100.00 Very High Very High Very High
Sepsis 189 99.84 Very High Very High Very High
Injury 28 99.32 Very High Very High Very High
Experimental Autoimmune Neuritis 8 97.08 Very High Very High Very High
Obesity 60 96.00 Very High Very High Very High
Insulin Resistance 60 92.64 High High
Stress 42 91.60 High High
Endotoxemia 6 78.12 Quite High
Immunization 4 77.08 Quite High
Pulmonary Disease 2 75.68 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Increased phosphorylation of c-Jun NH (2)-terminal protein kinase in the sciatic nerves of Lewis rats with experimental autoimmune neuritis.
Positive_regulation (Increased) of Phosphorylation (phosphorylation) of Jun in sciatic nerves associated with experimental autoimmune neuritis, sciatic nerve and neuritis
1) Confidence 0.67 Published 2006 Journal J. Vet. Sci. Section Title Doc Link 16434843 Disease Relevance 0.97 Pain Relevance 0.80
In addition, C2 ceramide also increased AP-1 proteins, such as Fra-1, c-Jun, JunB and JunD, and phosphorylation of CREB.
Positive_regulation (increased) of Phosphorylation (phosphorylation) of c-Jun
2) Confidence 0.22 Published 2001 Journal Brain Res. Section Abstract Doc Link 11382404 Disease Relevance 0 Pain Relevance 0
This comes as a surprise, as it is presumed that Jun can be phosphorylated only by the action of JNK.
Positive_regulation (presumed) of Phosphorylation (phosphorylated) of Jun
3) Confidence 0.22 Published 2008 Journal BMC Immunol Section Body Doc Link PMC2525626 Disease Relevance 0 Pain Relevance 0.07
In addition, C2 ceramide also increased AP-1 proteins, such as Fra-1, c-Jun, JunB and JunD, and phosphorylation of CREB.
Positive_regulation (increased) of Phosphorylation (phosphorylation) of AP-1
4) Confidence 0.19 Published 2001 Journal Brain Res. Section Abstract Doc Link 11382404 Disease Relevance 0 Pain Relevance 0
Another TLR4 downstream pathway by which atorvastatin could attenuate the inflammatory response induced by sepsis is through JNK, a serine kinase that is responsible for activation of the inflammatory pathway by phosphorylation of the c-Jun and ATF2 transcription factors [59], [60].
Positive_regulation (activation) of Phosphorylation (phosphorylation) of c-Jun associated with inflammatory response, inflammation and sepsis
5) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2997789 Disease Relevance 0.90 Pain Relevance 0.17
JNK activation was determined by monitoring phosphorylation of JNK (Thr183 and Tyr185) and c-Jun (Ser63), which is a substrate of JNK.
Positive_regulation (substrate) of Phosphorylation (phosphorylation) of c-Jun
6) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2997789 Disease Relevance 0.80 Pain Relevance 0.12
Consistent with JNK activation, c-Jun phosphorylation was induced by sepsis and reversed by atorvastatin in the tissues investigated (Fig. 4D–F).
Positive_regulation (induced) of Phosphorylation (phosphorylation) of c-Jun associated with sepsis
7) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2997789 Disease Relevance 0.69 Pain Relevance 0.03
Davis [19] reported that activated JNK is capable of binding the NH2-terminal activation domain of c-Jun, activating AP-1 by phosphorylating its component c-Jun.
Positive_regulation (activating) of Phosphorylation (phosphorylating) of c-Jun
8) Confidence 0.07 Published 2004 Journal Respir Res Section Body Doc Link PMC538282 Disease Relevance 0.60 Pain Relevance 0.18
ATF3 is a member of the CREB family and its rapid expression after injury in neurons is preceded by a fast upregulation of JNK and phophorylation of c-jun [12,13,16].
Positive_regulation (upregulation) of Phosphorylation (phophorylation) of c-jun in neurons associated with injury
9) Confidence 0.03 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2556676 Disease Relevance 0.10 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox