INT76925

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Context Info
Confidence 0.57
First Reported 1998
Last Reported 2009
Negated 0
Speculated 0
Reported most in Abstract
Documents 6
Total Number 7
Disease Relevance 2.90
Pain Relevance 1.25

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

endoplasmic reticulum (G6pc)
G6pc (Mus musculus)
Pain Link Frequency Relevance Heat
Paracetamol 17 96.02 Very High Very High Very High
tolerance 38 95.16 Very High Very High Very High
palliative 2 88.28 High High
Analgesic 2 43.20 Quite Low
cytokine 4 5.00 Very Low Very Low Very Low
anesthesia 4 5.00 Very Low Very Low Very Low
agonist 2 5.00 Very Low Very Low Very Low
Kinase C 2 5.00 Very Low Very Low Very Low
Immobilon 2 5.00 Very Low Very Low Very Low
imagery 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Glycogen Storage Disease 4 99.20 Very High Very High Very High
Hypoglycemia 4 98.44 Very High Very High Very High
Impaired Glucose Tolerance 28 95.16 Very High Very High Very High
Targeted Disruption 34 91.60 High High
Diabetes Mellitus 52 89.20 High High
Obesity 20 88.16 High High
Sprains And Strains 2 85.76 High High
Hepatotoxicity 5 85.72 High High
Lipidosis 6 84.52 Quite High
Disorder Of Lipid Metabolism 6 78.32 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
APAP at this dose was markedly hepatotoxic to mice when administered at 20:00 h as determined by increases in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, and by decreases in hepatic glucose-6-phosphatase (G-6-Pase) activity.
Negative_regulation (decreases) of G-6-Pase associated with paracetamol
1) Confidence 0.57 Published 1998 Journal Toxicology Section Abstract Doc Link 9704905 Disease Relevance 0.16 Pain Relevance 0.96
Glycogen storage disease type Ia (GSDIa) is caused by a genetic defect in the hepatic enzyme glucose-6-phosphatase (G6Pase-alpha), which manifests as life-threatening hypoglycemia with related metabolic complications.
Negative_regulation (defect) of G6Pase-alpha associated with hypoglycemia and glycogen storage disease
2) Confidence 0.43 Published 2009 Journal Lab. Invest. Section Abstract Doc Link 19581879 Disease Relevance 0.64 Pain Relevance 0.05
In addition, our data reveal that adult mice lacking G6Pase-alpha are able to mate and produce viable offspring.
Negative_regulation (lacking) of G6Pase-alpha
3) Confidence 0.43 Published 2009 Journal Lab. Invest. Section Abstract Doc Link 19581879 Disease Relevance 0.83 Pain Relevance 0.09
These data suggest that insulin signaling through AKT-dependent FOXO1 phosphorylation contributes to the observed reduction in steady-state mRNA levels for gluconeogenic genes such as G6pc and Pck1.


Negative_regulation (reduction) of G6pc
4) Confidence 0.39 Published 2008 Journal Diabetes Section Body Doc Link PMC2494684 Disease Relevance 0.12 Pain Relevance 0
and enzymes (G6Pase) implicated in gluconeogenesis were downregulated after treatment.
Negative_regulation (downregulated) of G6Pase
5) Confidence 0.38 Published 2008 Journal Diabetes Section Abstract Doc Link PMC2494684 Disease Relevance 0.37 Pain Relevance 0
It also modestly reduced the expression level of G6Pase, although the effect was not statistically significant.
Negative_regulation (reduced) of G6Pase
6) Confidence 0.35 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.26 Pain Relevance 0.06
reduces hepatic glucose output along with downregulation of PEPCK and G6Pase expression (33).
Negative_regulation (downregulation) of G6Pase
7) Confidence 0.15 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.45 Pain Relevance 0.08

General Comments

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