INT112131

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Context Info
Confidence 0.49
First Reported 2003
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 10
Total Number 11
Disease Relevance 9.95
Pain Relevance 1.85

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

endosome (Egfr) cell morphogenesis (Egfr) Golgi apparatus (Egfr)
endoplasmic reticulum (Egfr) intracellular (Egfr) enzyme binding (Egfr)
Anatomy Link Frequency
enterocytes 4
Egfr (Mus musculus)
Pain Link Frequency Relevance Heat
qutenza 12 99.74 Very High Very High Very High
cINOD 13 98.36 Very High Very High Very High
metalloproteinase 19 92.16 High High
antagonist 9 92.16 High High
Inflammation 58 91.20 High High
Inflammatory mediators 3 83.12 Quite High
imagery 13 33.84 Quite Low
Bile 1 26.88 Quite Low
COX2 9 25.00 Low Low
Kinase C 39 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Cancer 335 99.92 Very High Very High Very High
Targeted Disruption 15 98.64 Very High Very High Very High
Apoptosis 78 97.68 Very High Very High Very High
Colitis 134 96.16 Very High Very High Very High
Bullous Skin Disease 912 95.08 Very High Very High Very High
Metastasis 1 94.40 High High
Recurrence 2 91.56 High High
INFLAMMATION 63 91.20 High High
Stress 17 87.72 High High
Adhesions 155 84.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Increased activation of the EGFR-PI3K-Akt signaling pathway in tumors relative to Apc+/+ and ApcMin/+ enterocytes provides potential opportunities for therapeutic interventions to differentially suppress tumor formation, promotion, progression, and/or recurrence.
Positive_regulation (Increased) of Positive_regulation (activation) of EGFR-PI3K-Akt in enterocytes associated with cancer and recurrence
1) Confidence 0.49 Published 2004 Journal J. Biol. Chem. Section Abstract Doc Link 15294912 Disease Relevance 1.35 Pain Relevance 0.10
Increased activation of the EGFR-PI3K-Akt signaling pathway in tumors relative to Apc+/+ and ApcMin/+ enterocytes provides potential opportunities for therapeutic interventions to differentially suppress tumor formation, promotion, progression, and/or recurrence.
Positive_regulation (Increased) of Positive_regulation (activation) of EGFR-PI3K-Akt in enterocytes associated with cancer and recurrence
2) Confidence 0.49 Published 2004 Journal J. Biol. Chem. Section Abstract Doc Link 15294912 Disease Relevance 1.35 Pain Relevance 0.10
EGFR is overexpressed and activated in a variety of tumors and provides an attractive target for anti-cancer therapy (reviewed in [9]).
Positive_regulation (overexpressed) of Positive_regulation (activated) of EGFR associated with cancer
3) Confidence 0.45 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2716529 Disease Relevance 0.92 Pain Relevance 0
TPA/capsaicin cotreatment caused EGFR tyrosine phosphorylation and activated EGFR downstream signaling, including ERKs and Akt in EGFR/WT, but not EGFR/KO cells.
Positive_regulation (caused) of Positive_regulation (activated) of EGFR associated with targeted disruption and qutenza
4) Confidence 0.45 Published 2010 Journal Cancer Res. Section Abstract Doc Link 20660715 Disease Relevance 0.83 Pain Relevance 0.86
Lastly, PGE 2 treatment increased mucosal expression of AR and Cox-2, thus inducing EGFR activation and forming a positive feedback mechanism to amplify mucosal Cox-2.


Positive_regulation (inducing) of Positive_regulation (activation) of EGFR
5) Confidence 0.41 Published 2010 Journal BMC Gastroenterol Section Abstract Doc Link PMC2912804 Disease Relevance 0.99 Pain Relevance 0.03
Mice treated with PGE 2 had increased expression of Cox-2 and the EGFR-ligand, AR, leading to increased phosphorylation and activation of EGFR, indicating positive feedback.
Positive_regulation (increased) of Positive_regulation (activation) of EGFR
6) Confidence 0.41 Published 2010 Journal BMC Gastroenterol Section Body Doc Link PMC2912804 Disease Relevance 1.14 Pain Relevance 0.09
Also, gastrin-dependent COX-2 expression did not require PKC activity, activation of ERK, or transactivation of EGFR.
Neg (not) Positive_regulation (require) of Positive_regulation (transactivation) of EGFR
7) Confidence 0.34 Published 2003 Journal J. Cell. Physiol. Section Abstract Doc Link 12891702 Disease Relevance 0.13 Pain Relevance 0.15
ADAM17 on the other hand, was upregulated by activation of the epidermal growth factor receptor (EGFR) and caused shedding of Dsg 2 (Bech-Serra et al. 2006; Santiago-Josefat et al. 2007).
Positive_regulation (upregulated) of Positive_regulation (activation) of epidermal growth factor receptor
8) Confidence 0.25 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.31 Pain Relevance 0.25
ADAM17 on the other hand, was upregulated by activation of the epidermal growth factor receptor (EGFR) and caused shedding of Dsg 2 (Bech-Serra et al. 2006; Santiago-Josefat et al. 2007).
Positive_regulation (upregulated) of Positive_regulation (activation) of EGFR
9) Confidence 0.25 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.31 Pain Relevance 0.25
The linker function of plakoglobin seems to be regulated by tyrosine phosphorylation of plakoglobin because following EGFR activation, phosphorylated plakoglobin remained associated with Dsg 2 but not with desmoplakin (Gaudry et al. 2001).
Positive_regulation (following) of Positive_regulation (activation) of EGFR
10) Confidence 0.24 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.35 Pain Relevance 0
transmembrane proteinases (ADAMs), activation of GPCRs, EGFR transactivation,
Positive_regulation (activation) of Positive_regulation (transactivation) of EGFR
11) Confidence 0.13 Published 2008 Journal PPAR Research Section Body Doc Link PMC2440494 Disease Relevance 0.28 Pain Relevance 0.03

General Comments

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