INT228790

Context Info Confidence 0.41 First Reported 2008 Last Reported 2010 Negated 0 Speculated 0 Reported most in Body Documents 4 Total Number 4 Disease Relevance 0.58 Pain Relevance 0.15

nucleolus (Smad7) plasma membrane (Smad7) nucleus (Smad7) intracellular (Smad7) protein complex (Smad7) cytoplasm (Smad7)

Smad7 (Mus musculus)

Pain Link Frequency Relevance Heat Inflammation 25 86.64 cytokine 11 65.12 imagery 4 26.12 fibrosis 7 5.00 cINOD 3 5.00 chemokine 3 5.00 Glutamate receptor 3 5.00 anesthesia 2 5.00 ketamine 1 5.00

Disease Link Frequency Relevance Heat INFLAMMATION 28 86.64 Repression 3 82.60 Keloid Scars 4 75.60 Burns 10 74.96 Stress 6 73.76 Apoptosis 18 59.76 Cancer 16 50.00 Fibrosis 8 5.00 Dna Damage 3 5.00 Chromosome Aberrations 3 5.00

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

observation was the induction of MADH7 in all the cell lines exposed to

Positive_regulation (induction) of MADH7

1) Confidence 0.41 Published 2008 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2276817 Disease Relevance 0.13 Pain Relevance 0.06

Thus, we postulate that suppression of myofibroblasts by TSA is due to the suppression of Smad activity by the upregulation of Smad7 and TGIF and inhibition of extracellular deposition of fibronectin.

Positive_regulation (upregulation) of Smad7

2) Confidence 0.30 Published 2010 Journal Molecular Vision Section Body Doc Link PMC3013068 Disease Relevance 0.31 Pain Relevance 0.08

The most prominent gene induction was seen for MADH7,

Positive_regulation (induction) of MADH7

3) Confidence 0.27 Published 2008 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2276817 Disease Relevance 0 Pain Relevance 0

MADH7 was upregulated at 8 hours, and its expression level

Positive_regulation (upregulated) of MADH7

4) Confidence 0.27 Published 2008 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2276817 Disease Relevance 0.14 Pain Relevance 0

General Comments

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