INT187492

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Context Info
Confidence 0.05
First Reported 2005
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 9
Total Number 9
Disease Relevance 1.74
Pain Relevance 1.88

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

cytosol (ATIC) mitochondrion (ATIC) small molecule metabolic process (ATIC)
Anatomy Link Frequency
respiratory 1
ATIC (Homo sapiens)
Pain Link Frequency Relevance Heat
adenocard 26 99.12 Very High Very High Very High
cytokine 179 97.52 Very High Very High Very High
Inflammation 142 97.16 Very High Very High Very High
Inflammatory response 28 97.16 Very High Very High Very High
methotrexate 105 96.08 Very High Very High Very High
agonist 4 93.60 High High
Inflammatory mediators 44 83.48 Quite High
Arthritis 28 81.44 Quite High
Glutamate 2 68.08 Quite High
antagonist 4 64.48 Quite High
Disease Link Frequency Relevance Heat
Stress 78 97.60 Very High Very High Very High
INFLAMMATION 218 97.16 Very High Very High Very High
Cancer 11 91.24 High High
Death 25 90.84 High High
Arthritis 4 81.44 Quite High
Rheumatoid Arthritis 26 81.40 Quite High
Appetite Loss 28 68.00 Quite High
Toxicity 55 67.64 Quite High
Disease 157 65.20 Quite High
Juvenile Chronic Polyarthritis 23 50.00 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
MTX polyglutamates inhibit the action of amino-imidazole-carboxamidoadenosine-ribonucleotide transformylase (AICAR transformylase) more potently than enzymes involved in purine synthesis, causing an accumulation of AICAR and its metabolites.
Positive_regulation (accumulation) of AICAR associated with methotrexate
1) Confidence 0.05 Published 2008 Journal Rheumatology (Oxford, England) Section Body Doc Link PMC2468887 Disease Relevance 0.53 Pain Relevance 0.77
These observations indicate that AICAR activation of AMP kinase by phosphorylation of its catalytic subunits (Thr-172 of ?
Positive_regulation (activation) of AICAR
2) Confidence 0.05 Published 2005 Journal J Neuroinflammation Section Body Doc Link PMC1262754 Disease Relevance 0.07 Pain Relevance 0.13
In summary, the use of WT and RG cells allows us to distinguish several different mechanisms by which AMPK can be activated, of which the first three cause indirect activation by increasing cellular AMP: (1) inhibition of the respiratory chain (biguanides, galegine, troglitazone, phenobarbital, berberine), (2) inhibition of the mitochondrial ATP synthase (oligomycin, resveratrol), (3) inhibition of glycolysis (2-deoxyglucose), (4) increasing cytoplasmic Ca2+ (A23187), (5) intracellular conversion into an AMP mimetic (AICAR), and (6) direct binding to AMPK at a site distinct from the AMP site (A769662).
Positive_regulation (increasing) of AICAR in respiratory
3) Confidence 0.05 Published 2010 Journal Cell Metabolism Section Body Doc Link PMC2935965 Disease Relevance 0.17 Pain Relevance 0
Anti-oxidant functions of AICAR on LPS, A?
Positive_regulation (functions) of AICAR
4) Confidence 0.04 Published 2005 Journal J Neuroinflammation Section Body Doc Link PMC1262754 Disease Relevance 0.47 Pain Relevance 0.33
Inside the cell (in vivo) AICAR is converted to ZMP (an analog of AMP) which activates AMP kinase kinase (AMPKK) which in turn activates AMP kinase (AMPK) by phosphorylation on residues Thr 172 of the ?
Positive_regulation (converted) of AICAR
5) Confidence 0.04 Published 2005 Journal J Neuroinflammation Section Body Doc Link PMC1262754 Disease Relevance 0.10 Pain Relevance 0.08
peptide treatment, were restored to significant levels with AICAR treatment (fig. 7), thereby confirming AICAR's potential to balance the cellular redox status.


Positive_regulation (confirming) of AICAR
6) Confidence 0.04 Published 2005 Journal J Neuroinflammation Section Body Doc Link PMC1262754 Disease Relevance 0 Pain Relevance 0.03
To test the role of a single session of exercise on AICAR-increased food intake, AICAR (2 mM) or its vehicle were administered (i.c.v.) to control and exercised animals. 12-hour total food intake was measured after exercise.
Positive_regulation (increased) of AICAR
7) Confidence 0.03 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2585815 Disease Relevance 0.07 Pain Relevance 0.05
In exercised rats, AICAR (2 mM) did not cause any acute change in food intake but, in the control group, AICAR (2 mM) increased food intake by 32% (Figure 3a), suggesting that AICAR is not effective in exercised rats.
Neg (not) Positive_regulation (increased) of AICAR
8) Confidence 0.03 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2585815 Disease Relevance 0.06 Pain Relevance 0.04
Subsequently, the list of target genes has been extended to include amino-imidazole carboxamide ribonucleotide (AICAR) transformylase (gene name, ATIC), which inhibits de novo purine synthesis and promotes the accumulation of AICAR ribotide, inhibiting adenosine deaminase and leading to a build up of adenosine, a potent anti-inflammatory agent [32, 33].
Positive_regulation (accumulation) of AICAR associated with adenocard and inflammation
9) Confidence 0.02 Published 2010 Journal Human Genomics and Proteomics : HGP Section Body Doc Link PMC2958653 Disease Relevance 0.28 Pain Relevance 0.45

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