INT322764

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Context Info
Confidence 0.27
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 0.85
Pain Relevance 0.15

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

cytosol (GCLM) small molecule metabolic process (GCLM) cellular nitrogen compound metabolic process (GCLM)
GCLM (Homo sapiens)
Pain Link Frequency Relevance Heat
Glutamate 5 100.00 Very High Very High Very High
Central nervous system 1 40.48 Quite Low
Inflammation 3 6.68 Low Low
Potency 13 5.00 Very Low Very Low Very Low
Bioavailability 4 5.00 Very Low Very Low Very Low
methotrexate 2 5.00 Very Low Very Low Very Low
Bile 2 5.00 Very Low Very Low Very Low
cytokine 1 5.00 Very Low Very Low Very Low
member 8 1 5.00 Very Low Very Low Very Low
GABA receptor 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Autism 148 99.68 Very High Very High Very High
Stress 8 91.24 High High
Hepatocellular Cancer 4 69.24 Quite High
Toxicity 185 62.48 Quite High
Drug Induced Neurotoxicity 2 62.40 Quite High
Autoimmune Disease 1 34.04 Quite Low
Apoptosis 20 26.12 Quite Low
Liver Cancer 4 15.20 Low Low
Lymphatic System Cancer 1 10.64 Low Low
INFLAMMATION 4 6.68 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
GCLM is transcriptionally regulated in human HepG2 cells (Lee et al. 2006).
Regulation (regulated) of GCLM
1) Confidence 0.27 Published 2009 Journal Neurotox Res Section Body Doc Link PMC3006666 Disease Relevance 0.66 Pain Relevance 0.10
The enzymes involved in the synthesis of GSH (glutamate-cysteine ligase and GSH synthetase) are also present and can be up regulated by exogenous chemicals [15].
Regulation (regulated) of glutamate-cysteine ligase associated with glutamate
2) Confidence 0.01 Published 2010 Journal Combinatorial Chemistry & High Throughput Screening Section Body Doc Link PMC2908937 Disease Relevance 0.19 Pain Relevance 0.05

General Comments

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