INT192965

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Context Info
Confidence 0.74
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 15
Total Number 15
Disease Relevance 7.05
Pain Relevance 1.68

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

cell proliferation (Stat3) signal transduction (Stat3) plasma membrane (Stat3)
nucleus (Stat3) DNA binding (Stat3) transcription factor binding (Stat3)
Anatomy Link Frequency
nucleus 7
macrophage 1
liver 1
NK cells 1
lung 1
Stat3 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammatory mediators 4 99.84 Very High Very High Very High
Inflammation 154 98.32 Very High Very High Very High
fibrosis 108 96.72 Very High Very High Very High
Arthritis 19 88.28 High High
cytokine 146 88.04 High High
dexamethasone 9 85.40 High High
cINOD 9 81.88 Quite High
psoriasis 92 81.60 Quite High
Inflammatory response 19 78.04 Quite High
tolerance 49 76.80 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 177 99.84 Very High Very High Very High
Cancer 839 98.74 Very High Very High Very High
Yersinia Infection 5 97.64 Very High Very High Very High
Pulmonary Fibrosis 73 96.92 Very High Very High Very High
Stomach Cancer 10 94.64 High High
Adhesions 7 92.20 High High
Metastasis 240 91.32 High High
Skin Cancer 64 90.88 High High
Apoptosis 92 90.76 High High
Arthritis 13 88.28 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Besides these paracrine (or cell-extrinsic) pathways, activation of (proto-)oncogenes, inactivation of tumour-suppressor genes, chromosomal rearrangement/amplification and other genetic events in neoplastic cells either directly trigger Stat3 activation, or the release of inflammatory mediators as part of an autocrine (or cell-intrinsic) pathway.
Localization (release) of Stat3 associated with inflammatory mediators and cancer
1) Confidence 0.74 Published 2010 Journal Cell Div Section Body Doc Link PMC2887830 Disease Relevance 0.86 Pain Relevance 0.26
Since Stat3 inhibition also blocks VEGF expression in tumours characterized by aberrant activation of Src [77], therapeutic targeting of Stat3 may inhibit neovascularisation in tumours associated with excessive signaling through epidermal growth factor receptor.
Localization (targeting) of Stat3 associated with cancer
2) Confidence 0.74 Published 2010 Journal Cell Div Section Body Doc Link PMC2887830 Disease Relevance 0.84 Pain Relevance 0
Also, the TLR2/TLR6 heterodimer is involved in phosphorylation or nuclear translocation of Stat3 induced by macrophage activating lipopeptide-2 or LcrV of Yersinia pestis [28], [29].
Localization (translocation) of Stat3 in macrophage associated with yersinia infection
3) Confidence 0.62 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2716531 Disease Relevance 0.68 Pain Relevance 0.04
These results are consensually supported by the studies in which TLR4 activation inhibits phosphorylation and nucleus translocation of Stat3 [21] and activated Stat3 inhibits TLR4 signaling in return via inhibiting transcriptional or translational activity of NF-?
Localization (translocation) of Stat3 in nucleus
4) Confidence 0.62 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2716531 Disease Relevance 1.32 Pain Relevance 0.11
B translocation to the nucleus via nuclear targeting sequences in STAT3, resulting in subsequent transcription of a subset of NF?
Localization (translocation) of STAT3 in nucleus
5) Confidence 0.57 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.15 Pain Relevance 0.11
Similar to the IL-6- plus IL-10- neutralizing Ab, the TLR2 shRNA markedly inhibited the expression, phosphorylation and nucleus translocation of Stat3, which were partially restored by rmIL-6 and rmIL-10 (Fig. 2D–F).
Localization (translocation) of Stat3 in nucleus
6) Confidence 0.54 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2716531 Disease Relevance 0.16 Pain Relevance 0
Similar to IL-6 and IL-10, Pam3Cys significantly promoted the expression, phosphorylation, and nucleus translocation of Stat3 in B16 cells (Fig. 2D–F).
Localization (translocation) of Stat3 in nucleus
7) Confidence 0.54 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2716531 Disease Relevance 0.17 Pain Relevance 0.05
In turn, the anti-IL-6 plus IL-10 Abs partially inhibited the Pam3Cys-stimulated expression, phosphorylation and nucleus translocation of Stat3 (Fig. 2D–F).
Localization (translocation) of Stat3 in nucleus
8) Confidence 0.54 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2716531 Disease Relevance 0.14 Pain Relevance 0
Immunoblot analyses for angiotensin II, AT1R, synaptophysin, and phosphorylated forms of ERK, Akt, and STAT3.
Localization (forms) of STAT3
9) Confidence 0.39 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.08 Pain Relevance 0.08
in inflammation upregulate the IL-6 expression (20), and IL-6 stimulation in the liver induces the translocation of activated STAT3 molecules to nuclei (21,22).
Localization (translocation) of STAT3 in liver associated with inflammation
10) Confidence 0.30 Published 2006 Journal Evidence-based Complementary and Alternative Medicine Section Body Doc Link PMC1475933 Disease Relevance 0.79 Pain Relevance 0.53
were observed when NK cells were co-incubated with UCLA-OSCSCs which released significantly lower levels of GM-CSF, IL-6 and IL-8 (Tables 1 and 2) and demonstrated decreased expression of phospho-Stat3, B7H1 and EGFR, and much lower constitutive NF?
Localization (released) of Stat3 in NK cells
11) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2905395 Disease Relevance 0.49 Pain Relevance 0.16
Targeted genes could be Ku (releasing BAX), STAT3, HSP90, p53, and various transcription factors.
Localization (releasing) of STAT3
12) Confidence 0.22 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2926634 Disease Relevance 0.17 Pain Relevance 0.03
In contrast to deletion of STAT-1 or STAT-6, STAT-3 deletion in mice is lethal and therefore little is known about the role of STAT-3 in lung fibrosis.
Localization (deletion) of STAT-3 in lung associated with fibrosis and pulmonary fibrosis
13) Confidence 0.22 Published 2010 Journal Fibrogenesis Tissue Repair Section Body Doc Link PMC2940818 Disease Relevance 0.52 Pain Relevance 0.21
1 and IL-23R chain are associated with intracellular proteins of the Janus kinase (Jak) family to induce downstream signaling, resulting in a sequence of phosphorylation processes activating signal transducer and activator of transcription (STAT) molecules, namely STAT1, STAT3, STAT4, and STAT5, which translocate into the nucleus where they bind DNA in the promoter region of target genes.24
Localization (translocate) of STAT3 in nucleus
14) Confidence 0.20 Published 2010 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2880344 Disease Relevance 0.33 Pain Relevance 0.08
This inhibition led to a decrease in the dimerisation of STAT3 and its translocation into the nucleus for transcriptional activation of many genes in a wide range of biological processes, including induction of immune response, oncogenesis, cell cycle control, development, cell adhesion, and differentiation [63].
Localization (translocation) of STAT3 in nucleus associated with adhesions
15) Confidence 0.19 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2926634 Disease Relevance 0.34 Pain Relevance 0.03

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