INT210403

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Context Info
Confidence 0.24
First Reported 2007
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 0.89
Pain Relevance 0.09

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

transferase activity, transferring glycosyl groups (FUT1) Golgi apparatus (FUT1) carbohydrate metabolic process (FUT1)
Anatomy Link Frequency
Kupffer cells 1
FUT1 (Homo sapiens)
Pain Link Frequency Relevance Heat
cytokine 22 92.72 High High
fibrosis 29 39.60 Quite Low
COX2 1 28.20 Quite Low
Inflammation 50 5.00 Very Low Very Low Very Low
Inflammatory response 11 5.00 Very Low Very Low Very Low
Bile 6 5.00 Very Low Very Low Very Low
chemokine 6 5.00 Very Low Very Low Very Low
alcohol 5 5.00 Very Low Very Low Very Low
antagonist 3 5.00 Very Low Very Low Very Low
Paracetamol 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Cirrhosis 155 100.00 Very High Very High Very High
Apoptosis 68 60.96 Quite High
Wound Healing 12 50.00 Quite Low
Stress 107 5.00 Very Low Very Low Very Low
INFLAMMATION 59 5.00 Very Low Very Low Very Low
Death 55 5.00 Very Low Very Low Very Low
Injury 47 5.00 Very Low Very Low Very Low
Fibrosis 45 5.00 Very Low Very Low Very Low
Liver Disease 44 5.00 Very Low Very Low Very Low
Hepatitis C Virus Infection 27 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We also determined the intrahepatic localization of both HSC-targeted forms of 15dPGJ2. 15dPGJ2-M6PHSA predominantly accumulated in the HSC (64%) and Kupffer cells (39%).
Phosphorylation (forms) of HSC in Kupffer cells associated with cirrhosis
1) Confidence 0.24 Published 2007 Journal Pharm Res Section Body Doc Link PMC1915609 Disease Relevance 0.61 Pain Relevance 0
In 2003, Bataller and coworkers [318] were the first to identify the presence of components of NOX in HSC/MFs, suggesting that the pro-fibrogenic action of Ang II, as already delineated in in vivo and in vitro studies [319,320], is dependent on the associated activation of NOX and the related ROS-dependent activation of MAPKs, phosphorylation of c-Akt and increased AP-1 DNA binding activity [318], events blocked by the specific NOX inhibitor DPI (diphenyl-phenyleneiodonium) or the inhibitor of Ang II type 1 receptor (AT1), losartan.
Phosphorylation (phosphorylation) of HSC
2) Confidence 0.08 Published 2008 Journal Fibrogenesis Tissue Repair Section Body Doc Link PMC2584013 Disease Relevance 0.27 Pain Relevance 0.09

General Comments

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