INT91463

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Context Info
Confidence 0.40
First Reported 2000
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 19
Total Number 22
Disease Relevance 17.70
Pain Relevance 4.60

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

nucleoplasm (NFKB2) extracellular matrix organization (NFKB2) DNA binding (NFKB2)
cytoplasm (NFKB2) cytosol (NFKB2) signal transduction (NFKB2)
Anatomy Link Frequency
muscle 2
chondrocytes 1
nucleus 1
epithelial cells 1
adipose tissue 1
NFKB2 (Homo sapiens)
Pain Link Frequency Relevance Heat
cytokine 193 99.54 Very High Very High Very High
Inflammation 532 99.24 Very High Very High Very High
corticosteroid 225 99.12 Very High Very High Very High
Inflammatory response 268 98.80 Very High Very High Very High
cINOD 14 98.58 Very High Very High Very High
Serotonin 91 90.32 High High
rheumatoid arthritis 4 90.32 High High
Pain 22 88.36 High High
agonist 6 86.20 High High
antagonist 22 83.84 Quite High
Disease Link Frequency Relevance Heat
Appetite Loss 361 99.84 Very High Very High Very High
Insulin Resistance 16 99.62 Very High Very High Very High
INFLAMMATION 854 99.24 Very High Very High Very High
Mesothelioma 47 98.66 Very High Very High Very High
Apoptosis 187 98.28 Very High Very High Very High
Infection 54 96.66 Very High Very High Very High
Frailty 14 95.72 Very High Very High Very High
Obesity 61 95.64 Very High Very High Very High
Congenital Anomalies 47 95.20 Very High Very High Very High
Apnoea 48 94.40 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We test the hypothesis that the activation of NFkB signaling module serves as the representative signaling controller of the pro-inflammatory genetic switch underpinning the manifestation of transcriptional responses.
Positive_regulation (activation) of NFkB associated with inflammation
1) Confidence 0.40 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2651450 Disease Relevance 0.79 Pain Relevance 0.54
Upon infection of epithelial cells, the bacteria either directly induce protection of the mitochondria by secreting T3SS effector proteins or indirectly protect the mitochondria by upregulating several eukaryotic genes including JUN, NFKB2, and BCL2.
Positive_regulation (upregulating) of NFKB2 in epithelial cells associated with infection
2) Confidence 0.29 Published 2010 Journal BMC Genomics Section Body Doc Link PMC2996966 Disease Relevance 0.86 Pain Relevance 0
The unifying hypothesis is that the response is triggered by the activation of the NFkB signaling module and corticosteroids serve as a template for assessing anti-inflammatory strategies.
Positive_regulation (activation) of NFkB associated with corticosteroid and inflammation
3) Confidence 0.27 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2651450 Disease Relevance 0.56 Pain Relevance 0.37
First, the “translation” of the active signaling complex (DR*) into biologically relevant signaling compartments; namely involving the activation of NFkB signaling module.
Positive_regulation (activation) of NFkB
4) Confidence 0.27 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2651450 Disease Relevance 0.79 Pain Relevance 0.44
The response is triggered by the activation of the NFkB signaling module as a result of the formation of an activating signal associated with the binding of LPS to appropriate receptors.
Positive_regulation (activation) of NFkB
5) Confidence 0.27 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2651450 Disease Relevance 0.55 Pain Relevance 0.34
The primary endpoint is overall survival.In preclinical mesothelioma models, the proteasome inhibitor bortezomib inhibits constitutive activation of NFkB and enhances the cytotoxicity of cisplatin and pemetrexed [49, 50].
Positive_regulation (activation) of NFkB associated with mesothelioma
6) Confidence 0.18 Published 2008 Journal Curr Treat Options Oncol Section Body Doc Link PMC2782121 Disease Relevance 0.88 Pain Relevance 0.09
Initial studies using animal models have demonstrated that NFkB is upregulated in CC increasing proteolysis and inducing apoptosis in myotubes [43, 44].
Positive_regulation (upregulated) of NFkB in myotubes associated with appetite loss and apoptosis
7) Confidence 0.13 Published 2010 Journal Curr Treat Options Oncol Section Body Doc Link PMC3016925 Disease Relevance 0.98 Pain Relevance 0
Although the etiopathogenesis of CC is poorly understood, studies have proposed that NFkB is upregulated in CC, modulating immune and inflammatory responses induce the cellular breakdown of muscle, resulting in sarcopenia.
Positive_regulation (upregulated) of NFkB in muscle associated with appetite loss, inflammatory response and frailty
8) Confidence 0.13 Published 2010 Journal Curr Treat Options Oncol Section Abstract Doc Link PMC3016925 Disease Relevance 1.58 Pain Relevance 0.12
to its receptors results in the activation of major transcription factors such as AP-1 and NFkB which in turn induce genes involved in acute and chronic inflammatory responses (9).
Positive_regulation (activation) of NFkB associated with inflammatory response
9) Confidence 0.12 Published 2006 Journal Journal of Korean Medical Science Section Body Doc Link PMC2721922 Disease Relevance 0.94 Pain Relevance 0.29
Cytokines such as IL-1 can also stimulate the NFkB binding molecule to activate NFkB [54-56], which induces the expression of cyclooxygenase-2 (COX-2), which consequently leads to tissue inflammation at the site where latent TB antigens are located.
Positive_regulation (stimulate) of NFkB associated with mycobacterial infection, inflammation and cytokine
10) Confidence 0.12 Published 2007 Journal AIDS Res Ther Section Body Doc Link PMC2216023 Disease Relevance 0.87 Pain Relevance 0.23
It has been suggested that insulin resistance, through both the activation of nuclear factor kappa B by increased levels of cytokines (i.e., IL-6 and TNF-alpha) and the releasing of free fatty acids by excess adipose tissue, is involved in the pathogenic mechanisms leading to SAHS in humans [17].
Positive_regulation (activation) of nuclear factor kappa B in adipose tissue associated with apnoea, obesity, insulin resistance and cytokine
11) Confidence 0.11 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2650786 Disease Relevance 1.95 Pain Relevance 0.12
effects) [37-39] GS was also shown, on chondrocytes, to directly inhibit the activation of the transcription factor nuclear factor-kappa B[38,39], thus preventing the activation of a gene required for osteoclastogenesis.
Positive_regulation (activation) of nuclear factor-kappa B in chondrocytes
12) Confidence 0.10 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2246236 Disease Relevance 0.13 Pain Relevance 0.08
Thus, whole plant yucca powder has powerful anti-inflammatory activity, mediated via inhibition of NFkB activation.
Positive_regulation (activation) of NFkB associated with inflammation
13) Confidence 0.09 Published 2006 Journal J Inflamm (Lond) Section Body Doc Link PMC1440857 Disease Relevance 0.94 Pain Relevance 0.47
Several recent laboratory studies have shown that n-3 fatty acid may attenuate protein degradation, potentially by preventing NFkB accumulation in the nucleus, preventing the degradation of muscle proteins.
Positive_regulation (accumulation) of NFkB in muscle
14) Confidence 0.09 Published 2010 Journal Curr Treat Options Oncol Section Abstract Doc Link PMC3016925 Disease Relevance 1.34 Pain Relevance 0.12
Several recent laboratory studies have shown that EPA may attenuate protein degradation, by preventing NFkB accumulation in the nucleus [43, 44].
Positive_regulation (accumulation) of NFkB in nucleus
15) Confidence 0.09 Published 2010 Journal Curr Treat Options Oncol Section Body Doc Link PMC3016925 Disease Relevance 0.93 Pain Relevance 0
IL-1beta induces p38 MAPK phosphorylation and activation of the nuclear factor-kappaB independently from each other.
Positive_regulation (activation) of nuclear factor-kappaB
16) Confidence 0.07 Published 2000 Journal J. Neurochem. Section Abstract Doc Link 11032891 Disease Relevance 0.46 Pain Relevance 0.11
activation of the transcription factor NFkB, which leads to the upregulation of
Positive_regulation (activation) of NFkB
17) Confidence 0.07 Published 2008 Journal Journal of Oncology Section Body Doc Link PMC2648637 Disease Relevance 0.78 Pain Relevance 0.20
reinforce NFkB activation and the ceramide pathway.
Positive_regulation (activation) of NFkB
18) Confidence 0.07 Published 2008 Journal Journal of Oncology Section Body Doc Link PMC2648637 Disease Relevance 0.57 Pain Relevance 0.23
was demonstrated to be a marker of NFkB activation [18], we studied the appearance of phospho-IkB (pIkB) upon PGN-ECndss treatment of HCE-T cells using western blot technique (Figure 3B).
Positive_regulation (activation) of NFkB in T cells
19) Confidence 0.05 Published 2008 Journal Molecular Vision Section Body Doc Link PMC2526096 Disease Relevance 0 Pain Relevance 0.04
It has been shown that steroids and nonsteroidal anti-inflammatory drugs are beneficial.22 Therefore, it is crucial to get a better insight in activation of NFkB and release of prostaglandins.
Positive_regulation (activation) of NFkB associated with inflammation and cinod
20) Confidence 0.05 Published 2008 Journal Eplasty Section Body Doc Link PMC2431646 Disease Relevance 0.89 Pain Relevance 0.17

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