INT103609

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Context Info
Confidence 0.11
First Reported 2002
Last Reported 2002
Negated 0
Speculated 0
Reported most in Abstract
Documents 1
Total Number 3
Disease Relevance 0.97
Pain Relevance 2.42

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

nucleolus (Sp1) nucleus (Sp1) intracellular (Sp1)
DNA binding (Sp1) transcription factor binding (Sp1) cytoplasm (Sp1)
Sp1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
cINOD 30 99.74 Very High Very High Very High
metalloproteinase 6 99.40 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 6 98.62 Very High Very High Very High
Repression 3 94.56 High High
Lung Cancer 3 93.36 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Promoter deletion and mutation analysis indicate that NSAIDs act via the Sp1 transcription factor binding site located between -91 and -84 in the MMP-2 promoter to suppress gene expression.
Transcription (transcription) of Sp1 associated with cinod
1) Confidence 0.11 Published 2002 Journal J. Biol. Chem. Section Abstract Doc Link 12087091 Disease Relevance 0.35 Pain Relevance 0.73
Nonsteroidal anti-inflammatory drugs inhibit matrix metalloproteinase-2 via suppression of the ERK/Sp1-mediated transcription.
Transcription (transcription) of Sp1 associated with inflammation, metalloproteinase and cinod
2) Confidence 0.06 Published 2002 Journal J. Biol. Chem. Section Title Doc Link 12087091 Disease Relevance 0.38 Pain Relevance 0.88
Collectively, our data suggest that NSAIDs inhibit MMP-2 by blocking ERK/Sp1-mediated transcription.
Transcription (transcription) of Sp1 associated with cinod
3) Confidence 0.06 Published 2002 Journal J. Biol. Chem. Section Abstract Doc Link 12087091 Disease Relevance 0.24 Pain Relevance 0.81

General Comments

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