INT109914

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.56
First Reported 2001
Last Reported 2009
Negated 1
Speculated 1
Reported most in Body
Documents 16
Total Number 17
Disease Relevance 7.64
Pain Relevance 3.27

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

cytosol (MAPK9) nucleoplasm (MAPK9) mitochondrion (MAPK9)
nucleus (MAPK9) transcription factor binding (MAPK9) response to stress (MAPK9)
Anatomy Link Frequency
joint 1
monocytes 1
MOLT-4 1
MAPK9 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 42 99.36 Very High Very High Very High
dexamethasone 8 99.22 Very High Very High Very High
cINOD 40 98.84 Very High Very High Very High
Enkephalin 13 96.80 Very High Very High Very High
Paracetamol 13 93.60 High High
cytokine 23 87.84 High High
chemokine 10 87.28 High High
Osteoarthritis 42 85.72 High High
rheumatoid arthritis 34 84.68 Quite High
COX-2 inhibitor 5 57.00 Quite High
Disease Link Frequency Relevance Heat
Apoptosis 252 100.00 Very High Very High Very High
Stress 111 100.00 Very High Very High Very High
Death 32 99.84 Very High Very High Very High
Nerve Sheath Neoplasms 110 99.76 Very High Very High Very High
INFLAMMATION 54 99.36 Very High Very High Very High
Shock 27 99.32 Very High Very High Very High
Osteoarthritis 46 97.54 Very High Very High Very High
Cancer 127 94.76 High High
Colon Cancer 13 92.20 High High
Metastasis 3 87.84 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Furthermore, it increased the phosphorylation level of c-Jun N-terminal kinase and induced apoptosis in MOLT-4 cells.
Positive_regulation (increased) of c-Jun N-terminal kinase in MOLT-4 associated with apoptosis
1) Confidence 0.56 Published 2009 Journal Cancer Sci. Section Abstract Doc Link 19141128 Disease Relevance 1.34 Pain Relevance 1.05
In addition, anti-inflammatory drugs dexamethasone (DEX) and cyclosporin A (CSA) both blocked activation of JNKS/SAPK and the cell-cell contact induced production of hRPE IL-8 and MCP-1, while activation of p38 and ERK was only inhibited by DEX, but not by CSA.
Positive_regulation (activation) of SAPK associated with inflammation, cinod and dexamethasone
2) Confidence 0.49 Published 2003 Journal Exp. Eye Res. Section Abstract Doc Link 12697421 Disease Relevance 0.15 Pain Relevance 0.40
In the same cell type neither IL-1beta-dependent SAPK activation nor IL-6-induced STAT3 phosphorylation is affected by the drug.
Neg (neither) Positive_regulation (activation) of SAPK
3) Confidence 0.37 Published 2003 Journal Neurosci. Lett. Section Abstract Doc Link 14664905 Disease Relevance 0 Pain Relevance 0.48
As this result suggests an effect at transcriptional level, we examined whether the drug interferes with the activation of nuclear factor (NF)-kappaB and STAT3 transcription factors and with SAPK signal transducing factor.
Spec (whether) Positive_regulation (activation) of SAPK
4) Confidence 0.37 Published 2003 Journal Neurosci. Lett. Section Abstract Doc Link 14664905 Disease Relevance 0 Pain Relevance 0.39
Previously we have shown that VEGF stimulation of HIMECs leads to a marked phosphorylation and activation of all three MAPK family members (p44/42 MAPK, stress-activated protein kinase (SAPK)/JNK and p38 MAPK).25 To investigate whether MAPK pathways play a role in VEGF induction of COX-2, HIMECs were pretreated with specific MAPK inhibitors then activated with VEGF.
Positive_regulation (activation) of SAPK associated with stress
5) Confidence 0.22 Published 2008 Journal Gut Section Body Doc Link PMC2582343 Disease Relevance 0.10 Pain Relevance 0.03
Stimulation of hRPE cells by monocytes resulted in prominent increases in p38, ERK1/2 and JNK/SAPK phosphorolation, IkappaBalpha degradation, and NF-kappaB nuclear translocation.
Positive_regulation (increases) of SAPK in monocytes
6) Confidence 0.21 Published 2003 Journal Exp. Eye Res. Section Abstract Doc Link 12697421 Disease Relevance 0.14 Pain Relevance 0.23
In contrast, synovial membranes of degenerative joint disease show almost no MAPK/SAPK activation [58,59], indicating the essential role of inflammation as the basis for synovial MAPK/SAPK activation.
Positive_regulation (activation) of SAPK in joint associated with inflammation and osteoarthritis
7) Confidence 0.18 Published 2001 Journal Arthritis Res Section Body Doc Link PMC128883 Disease Relevance 0.60 Pain Relevance 0.19
Preceding cell death, TRAIL activated nuclear factor kappaB, c-Jun N-terminal kinase, p38 and p42/44.
Positive_regulation (activated) of c-Jun N-terminal kinase associated with death
8) Confidence 0.16 Published 2009 Journal FEBS J. Section Abstract Doc Link 19895579 Disease Relevance 1.00 Pain Relevance 0
SAPK/JNK and caspase-3 activation
Positive_regulation (activation) of SAPK
9) Confidence 0.15 Published 2004 Journal Cancer Cell Int Section Body Doc Link PMC425591 Disease Relevance 0.44 Pain Relevance 0
also markedly increased the SAPK/JNK (p46 and p54), particularly the level of the p46 isoforms.
Positive_regulation (increased) of SAPK
10) Confidence 0.14 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2483463 Disease Relevance 0.37 Pain Relevance 0.15
The stress-activated protein kinase/ Jun-terminal kinase SAPK/JNK, a mediator of apoptosis, was activated (phosphorylated) 16 h after treatment with either of the Sulindac metabolites (not shown), and increased further after 24 h and 48 h (Fig. 6).
Positive_regulation (kinase) of SAPK associated with stress and apoptosis
11) Confidence 0.11 Published 2004 Journal Cancer Cell Int Section Body Doc Link PMC425591 Disease Relevance 0.45 Pain Relevance 0
The stress-activated protein kinase/ Jun-terminal kinase SAPK/JNK, a mediator of apoptosis, was activated (phosphorylated) 16 h after treatment with either of the Sulindac metabolites (not shown), and increased further after 24 h and 48 h (Fig. 6).
Positive_regulation (activated) of SAPK associated with stress and apoptosis
12) Confidence 0.11 Published 2004 Journal Cancer Cell Int Section Body Doc Link PMC425591 Disease Relevance 0.46 Pain Relevance 0
Furthermore, Sulindac metabolites showed low activation of caspase-3, a common downstream regulator of SAPK/JNK [23,33].
Positive_regulation (activation) of SAPK
13) Confidence 0.10 Published 2004 Journal Cancer Cell Int Section Body Doc Link PMC425591 Disease Relevance 0.74 Pain Relevance 0.16
In MPNST-cells, the activation of phospho-SAPK/JNK preceded apoptosis and reached its peak at 24 h treatment, while the observed apoptosis rate still increased after 48 h of treatment, indicating a causative association.
Positive_regulation (activation) of SAPK associated with nerve sheath neoplasms and apoptosis
14) Confidence 0.10 Published 2004 Journal Cancer Cell Int Section Body Doc Link PMC425591 Disease Relevance 0.74 Pain Relevance 0.11
As expected, we observed that PEITC specifically inhibited the activating phosphorylation of SAPK induced by hyperosmotic shock using sorbitol (Figure 8, Panel A), consistent with the inhibition seen by in vitro kinase assay.
Positive_regulation (induced) of SAPK associated with shock
15) Confidence 0.10 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.52 Pain Relevance 0
These results demonstrate that MEKK1 is directly modified and inhibited by ITCs, and that this correlates with inhibition of downstream activation of SAPK.
Positive_regulation (activation) of SAPK
16) Confidence 0.10 Published 2007 Journal BMC Cancer Section Abstract Doc Link PMC2071920 Disease Relevance 0 Pain Relevance 0
It directly phosphorylates and activates the SEK1 protein kinase, leading to activation of the stress activated protein kinase/jun N terminal kinase (SAPK/JNK) [1,2].
Positive_regulation (activation) of SAPK associated with stress
17) Confidence 0.10 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.59 Pain Relevance 0.09

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox