INT119891

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Context Info
Confidence 0.59
First Reported 1999
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 4
Total Number 7
Disease Relevance 2.67
Pain Relevance 1.98

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

endosome (Cftr) transport (Cftr) ATPase activity (Cftr)
enzyme binding (Cftr) protein complex (Cftr) transmembrane transport (Cftr)
Anatomy Link Frequency
Caco-2 2
Cftr (Mus musculus)
Pain Link Frequency Relevance Heat
cINOD 12 99.90 Very High Very High Very High
aspirin 4 99.38 Very High Very High Very High
fibrosis 145 93.56 High High
Inflammation 16 90.40 High High
Chronic pancreatitis 1 50.16 Quite High
abdominal pain 4 42.56 Quite Low
Disease Link Frequency Relevance Heat
INFLAMMATION 20 98.90 Very High Very High Very High
Disease 11 98.88 Very High Very High Very High
Cystic Fibrosis 145 93.56 High High
Stress 4 84.40 Quite High
Congenital Anomalies 24 74.40 Quite High
Disorder Of Lipid Metabolism 48 53.28 Quite High
Pancreatitis 1 50.16 Quite High
Infection 24 45.40 Quite Low
Appetite Loss 8 44.12 Quite Low
Abdominal Pain 4 42.56 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The present study was undertaken to determine whether three nonsteroidal anti-inflammatory drugs (NSAIDs) (aspirin, ibuprofen, and indomethacin) modulate CFTR gene expression in T-84 cells.
Regulation (modulate) of Gene_expression (expression) of CFTR gene associated with aspirin, inflammation and cinod
1) Confidence 0.59 Published 1999 Journal Mediators Inflamm Section Abstract Doc Link PMC1781806 Disease Relevance 0.93 Pain Relevance 0.79
The results indicate that NSAIDs can regulate both CFTR gene expression and the function of CFTR-related chloride transport, and suggest that NSAIDs act via multiple transduction pathways.



Regulation (regulate) of Gene_expression (expression) of CFTR gene associated with cinod
2) Confidence 0.59 Published 1999 Journal Mediators Inflamm Section Abstract Doc Link PMC1781806 Disease Relevance 0.83 Pain Relevance 0.91
Influence of CFTR knockdown on FA uptake and output
Regulation (Influence) of Gene_expression (knockdown) of CFTR
3) Confidence 0.44 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2864762 Disease Relevance 0.11 Pain Relevance 0
In conclusion, our data bring novel and exciting insights on the effects of CFTR depletion, at a level seen in heterozygous subjects and even individuals carrying other CFTR mutations, on intestinal FA homeostasis.
Regulation (effects) of Gene_expression (depletion) of CFTR
4) Confidence 0.44 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2864762 Disease Relevance 0.06 Pain Relevance 0.03
Using the intestinal Caco-2/15 cell model, we could show that, reduced CFTR expression distinctively affects the different classes of FA.
Regulation (affects) of Gene_expression (expression) of CFTR in Caco-2
5) Confidence 0.44 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2864762 Disease Relevance 0.49 Pain Relevance 0.14
CFTR disruption did not influence the expression of PPAR-?
Neg (not) Regulation (influence) of Gene_expression (disruption) of CFTR
6) Confidence 0.44 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2864762 Disease Relevance 0.05 Pain Relevance 0.03
In addition, cSNPs may be responsible for variation in the phenotypic expression of CFTR mutations.
Regulation (responsible) of Gene_expression (expression) of CFTR
7) Confidence 0.27 Published 2004 Journal Hum. Mutat. Section Abstract Doc Link 15241793 Disease Relevance 0.20 Pain Relevance 0.08

General Comments

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