INT179814

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.06
First Reported 2004
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 5
Disease Relevance 3.38
Pain Relevance 0.85

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

signal transduction (Ecm1) extracellular space (Ecm1) extracellular region (Ecm1)
proteinaceous extracellular matrix (Ecm1) enzyme binding (Ecm1) signal transducer activity (Ecm1)
Anatomy Link Frequency
basement membrane 2
Ecm1 (Mus musculus)
Pain Link Frequency Relevance Heat
metalloproteinase 33 98.46 Very High Very High Very High
Bile 53 76.96 Quite High
Inflammation 146 72.64 Quite High
cytokine 44 46.88 Quite Low
Mechanotransduction 1 46.56 Quite Low
ischemia 11 20.16 Low Low
fibrosis 17 18.72 Low Low
chemokine 24 5.00 Very Low Very Low Very Low
Inflammatory response 21 5.00 Very Low Very Low Very Low
antagonist 19 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Edema 5 99.80 Very High Very High Very High
Breast Cancer 18 99.54 Very High Very High Very High
Adhesions 11 99.16 Very High Very High Very High
Stress 34 98.76 Very High Very High Very High
Apoptosis 69 97.80 Very High Very High Very High
Cancer 32 96.16 Very High Very High Very High
Atherosclerosis 35 93.32 High High
Nicotine Addiction 49 88.64 High High
Hepatotoxicity 4 86.28 High High
Pulmonary Disease 144 85.96 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
While not directly supporting a role in ECM degradation, these interactions suggest that IL-11 is involved in regulating the balance between MMP and TIMP activity in the tissue.


Positive_regulation (role) of Protein_catabolism (degradation) of ECM associated with metalloproteinase
1) Confidence 0.06 Published 2004 Journal Reprod Biol Endocrinol Section Body Doc Link PMC535545 Disease Relevance 0 Pain Relevance 0.34
Our data in cultured VSMCs show that statins upregulate the profibrotic mediator CTGF, the inhibitor of ECM degradation PAI-1, and collagen production, all of them regulated by Smads [7], [29], [30].
Positive_regulation (upregulate) of Protein_catabolism (degradation) of ECM
2) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2597201 Disease Relevance 0.52 Pain Relevance 0.03
Possible mechanisms by which PAI-1 promotes breast cancer include prevention of excess ECM degradation, modulation of cell adhesion, a role in angiogenesis, and the stimulation of cell proliferation [3].
Positive_regulation (excess) of Protein_catabolism (degradation) of ECM associated with breast cancer and adhesions
3) Confidence 0.04 Published 2008 Journal BMC Cancer Section Body Doc Link PMC2580770 Disease Relevance 1.42 Pain Relevance 0.03
Increased proteolytic load due to MMP-9 has been attributed to increased neutrophil recruitment in the lungs that triggers degradation of ECM and basement membrane in the airways and lungs.
Positive_regulation (triggers) of Protein_catabolism (degradation) of ECM in basement membrane associated with metalloproteinase
4) Confidence 0.03 Published 2007 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2695202 Disease Relevance 0.65 Pain Relevance 0.36
Also, increased hepatic lipid peroxidation, a high oxidative stress marker [66], can occur with increased membrane permeability, increased degradation of components of the ECM and edema [70].
Positive_regulation (increased) of Protein_catabolism (degradation) of ECM associated with stress and edema
5) Confidence 0.03 Published 2008 Journal Fibrogenesis Tissue Repair Section Body Doc Link PMC2637833 Disease Relevance 0.78 Pain Relevance 0.10

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox