INT121818

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Context Info
Confidence 0.47
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 25
Total Number 25
Disease Relevance 11.16
Pain Relevance 3.67

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

nucleoplasm (STAT3) DNA binding (STAT3) cytoplasm (STAT3)
signal transducer activity (STAT3) cell proliferation (STAT3) cytosol (STAT3)
Anatomy Link Frequency
SH2 1
myocardium 1
cardiomyocytes 1
platelets 1
nucleus 1
STAT3 (Homo sapiens)
Pain Link Frequency Relevance Heat
spinal inflammation 164 99.76 Very High Very High Very High
Crohn's disease 108 99.76 Very High Very High Very High
spondylitis 8 99.32 Very High Very High Very High
opioid receptor 14 97.16 Very High Very High Very High
cytokine 102 96.84 Very High Very High Very High
Inflammation 191 95.36 Very High Very High Very High
psoriasis 16 95.04 Very High Very High Very High
cINOD 6 94.64 High High
agonist 132 93.36 High High
Gabapentin 1 85.00 Quite High
Disease Link Frequency Relevance Heat
Disease 300 99.76 Very High Very High Very High
Ankylosing Spondylitis 168 99.76 Very High Very High Very High
Inflammatory Bowel Disease 154 99.36 Very High Very High Very High
Apoptosis 115 98.26 Very High Very High Very High
Multiple Myeloma 167 95.92 Very High Very High Very High
Infection 44 95.52 Very High Very High Very High
Cancer 692 95.48 Very High Very High Very High
INFLAMMATION 195 95.36 Very High Very High Very High
Psoriasis 16 95.04 Very High Very High Very High
Arthritis 22 94.84 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Furthermore, we selected this particular marker of immune suppression because IL-2 has been shown to regulate FoxP3 expression in human CD4+CD25+ Tregs [48] by inducing STAT-3 binding of the first intron of the FoxP3 gene [20] and because STAT-3 inhibitors have been shown to inhibit Tregs [26,36].
STAT-3 Binding (binding) of
1) Confidence 0.47 Published 2009 Journal J Transl Med Section Body Doc Link PMC2777138 Disease Relevance 0.48 Pain Relevance 0.06
Association in STAT3 was detected at experiment-wise significance for 2 markers (rs744166, P?
STAT3 Binding (Association) of
2) Confidence 0.47 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2996314 Disease Relevance 0.49 Pain Relevance 0.16
The association with IL12B is of particular interest given the associations of IL23R and STAT3 with AS.
STAT3 Binding (associations) of associated with spinal inflammation
3) Confidence 0.47 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2996314 Disease Relevance 0.93 Pain Relevance 0.29
A mutation analysis of the 5'-TTCATGGAA-3' STAT1/3 element (palindrome underlined) was performed to determine nucleotide residues that are necessary for the binding of STAT1 and STAT3.
STAT3 Binding (binding) of
4) Confidence 0.46 Published 2004 Journal Mol. Pharmacol. Section Abstract Doc Link 15448191 Disease Relevance 0.12 Pain Relevance 0.30
STAT1 and STAT3 bound to a site located at nucleotide -1583 on the promoter of the human mu-opioid receptor gene, as shown by transient transfection experiments, electrophoretic mobility shift assays, and transcription factor decoy oligonucleotides.
STAT3 Binding (bound) of associated with opioid receptor
5) Confidence 0.46 Published 2004 Journal Mol. Pharmacol. Section Abstract Doc Link 15448191 Disease Relevance 0.21 Pain Relevance 0.51
SOCS3 can bind phosphotyrosines on the JAK2 receptors, physically blocking STAT3 binding, as well as biding to JAK2, directly blocking JAK kinase activity [50].
STAT3 Binding (binding) of
6) Confidence 0.45 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2696599 Disease Relevance 0 Pain Relevance 0.07
To evaluate whether the percent of PBMCs displaying p-STAT-3 correlated with immune suppression, we tested for a correlation between the percent of PBMCs displaying p-STAT-3 and the fraction of enhanced Tregs in the systemic circulation [35] especially since p-STAT-3 binds to the first intron of the FoxP3 gene [20] and because STAT-3 inhibitors have been shown to inhibit Tregs [26,36].


STAT-3 Binding (binds) of
7) Confidence 0.41 Published 2009 Journal J Transl Med Section Body Doc Link PMC2777138 Disease Relevance 0.74 Pain Relevance 0.06
Association of Variants at 1q32 and STAT3 with Ankylosing Spondylitis Suggests Genetic Overlap with Crohn's Disease

Ankylosing spondylitis (AS) is a common inflammatory arthritic condition.

STAT3 Binding (Association) of associated with spinal inflammation, spondylitis, inflammation, ankylosing spondylitis, disease and arthritis
8) Confidence 0.41 Published 2010 Journal PLoS Genetics Section Title Doc Link PMC2996314 Disease Relevance 1.57 Pain Relevance 0.75
Association with disease was also detected for 2 variants within STAT3 (rs6503695, P?
STAT3 Binding (rs6503695) of associated with disease
9) Confidence 0.36 Published 2010 Journal PLoS Genetics Section Abstract Doc Link PMC2996314 Disease Relevance 1.31 Pain Relevance 0.59
More specifically, IL-2 has been shown to regulate FoxP3 expression in human CD4+CD25+ Tregs by inducing STAT-3 binding of the first intron of the FoxP3 gene [20].
STAT-3 Binding (binding) of
10) Confidence 0.35 Published 2009 Journal J Transl Med Section Body Doc Link PMC2777138 Disease Relevance 0.60 Pain Relevance 0.06
Since both STAT3 and BMX exhibit similar redistribution and phosphorylation, these data and our in vivo observations showing a complex formation between BMX and STAT3 in PO myocardium strongly indicate that integrin-mediated BMX activation might serve as an upstream kinase for STAT3 activation in hypertrophying myocardium.
STAT3 Binding (formation) of in myocardium
11) Confidence 0.34 Published 2008 Journal International Journal of Biological Sciences Section Body Doc Link PMC2443357 Disease Relevance 0.20 Pain Relevance 0.04
However, upon RGD stimulation in this 3D model, STAT3 was recruited to the insoluble pellet fraction and P-STAT3 levels were increased both in the insoluble and soluble fractions (p<0.05).
STAT3 Binding (recruited) of
12) Confidence 0.34 Published 2008 Journal International Journal of Biological Sciences Section Body Doc Link PMC2443357 Disease Relevance 0 Pain Relevance 0
Our studies with adult cardiomyocytes in vitro demonstrate that in a 3D model, but not in a 2D model without FAC formation (data not shown), stimulation with an RGD peptide caused both BMX and STAT3 recruitment to the detergent insoluble fraction (CSK+MSK) and hyperphosphorylation.
STAT3 Binding (recruitment) of in cardiomyocytes
13) Confidence 0.34 Published 2008 Journal International Journal of Biological Sciences Section Body Doc Link PMC2443357 Disease Relevance 0.20 Pain Relevance 0.04
Thus, tyrosine phosphorylation of STAT3 promotes a particular homodimerization conformation involving its SH2 (Src-homology 2) domain enabling STAT3 to bind target genes during transcriptional activation, including pro-survival genes.6
STAT3 Binding (bind) of in SH2
14) Confidence 0.33 Published 2008 Journal International Journal of Biological Sciences Section Body Doc Link PMC2443357 Disease Relevance 0.09 Pain Relevance 0
By 1 wk RVPO, both STAT3 recruitment and phosphorylation were substantially reduced.
STAT3 Binding (recruitment) of
15) Confidence 0.33 Published 2008 Journal International Journal of Biological Sciences Section Body Doc Link PMC2443357 Disease Relevance 0 Pain Relevance 0
In the absence of androgens, MAPK and AKT kinases may induce AR phosphorylation and activation, whereas STAT3 can bind ligand-free AR and facilitate its translocation to the nucleus.
STAT3 Binding (bind) of in nucleus
16) Confidence 0.29 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2957443 Disease Relevance 0.30 Pain Relevance 0
(no. 18) IL-6, in addition to interacting directly with STAT3 (see above), also makes mature platelets more sensitive to activation by thrombin and platelet activating factor [43].
STAT3 Binding (interacting) of in platelets
17) Confidence 0.25 Published 2010 Journal Human Genomics and Proteomics : HGP Section Body Doc Link PMC2958630 Disease Relevance 0 Pain Relevance 0.11
Given that SNPs within CCR6, STAT3, JAK2, IL23R, IL12B, the IL22/IL26 and the IL2/IL21 gene cluster have been found to be associated with CD and or UC, we should take in mind the influence of these SNPs on Th17 cytokine profiles.
STAT3 Binding (associated) of associated with inflammatory bowel disease, crohn's disease and cytokine
18) Confidence 0.22 Published 2010 Journal BMC Immunol Section Body Doc Link PMC3016394 Disease Relevance 0.51 Pain Relevance 0.29
Processes that are activated by EGFR stimulation include signal transduction pathways for PI3K-Akt (related to survival and apoptosis evasion) and Ras-Raf-MEK-MAPK (relating to proliferation).15 In addition, there is an interaction between EGFR expression and signal transducers and activators of transcription 3 (eg, STAT3), which play a role in the regulation of transcription of genes involved in cell cycle progression such as Fos, Cyclin-D, CDC25A, c-Myc and Pim1 and the upregulation of antiapoptotic genes such as BCL2.16,17
STAT3 Binding (interaction) of associated with apoptosis
19) Confidence 0.21 Published 2010 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2921255 Disease Relevance 0.30 Pain Relevance 0
Wang and colleagues [211] showed that 15d-PGJ2 and troglitazone significantly inhibited Stat3 binding to its cognate response element and inhibited Stat3 binding to the promoters of c-MYC and MCL-1 thereby preventing transactivation of these Stat3 target genes.
Stat3 Binding (binding) of
20) Confidence 0.20 Published 2010 Journal PPAR Research Section Body Doc Link PMC2829627 Disease Relevance 0.60 Pain Relevance 0.09

General Comments

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