INT262799

Context Info Confidence 0.56 First Reported 2007 Last Reported 2010 Negated 0 Speculated 0 Reported most in Body Documents 6 Total Number 6 Disease Relevance 2.09 Pain Relevance 0.04

transport (Smad3) intracellular (Smad3) DNA binding (Smad3) protein complex (Smad3) cytoplasm (Smad3) nucleus (Smad3)

Anatomy Link Frequency nucleus 1 lens 1 Smad3 (Mus musculus)

Pain Link Frequency Relevance Heat Inflammation 26 78.04 fibrosis 10 45.52 Kinase C 2 25.00 anesthesia 7 5.00 cytokine 5 5.00 ketamine 5 5.00 Calcitonin gene-related peptide 3 5.00 ischemia 2 5.00 Neurotransmitter 2 5.00 isoflurane 2 5.00

Disease Link Frequency Relevance Heat Cataract 68 100.00 Injury 16 99.16 Repression 14 98.72 Burns 13 98.36 Retinal Diseases 4 85.24 Targeted Disruption 24 80.96 Apoptosis 67 79.08 INFLAMMATION 27 78.04 Ganglion Cysts 26 67.60 Sprains And Strains 2 55.20

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

Findings for the models described above, as well as the recently developed alkali burn model, are in contrast to earlier work by Saika and colleagues which showed that Smad3 deficient mice were resistant to ASC formation in response to lens injury [45].

Localization (formation) of Smad3 in lens associated with burns, injury and cataract

1) Confidence 0.56 Published 2007 Journal Molecular Vision Section Body Doc Link PMC2647562 Disease Relevance 1.06 Pain Relevance 0

Since Sox17 negatively regulated Smad3 transcriptional activity in reporter assays but did not influence Smad3 nuclear import, we sought to determine if the repression was mediated by influencing Smad3 DNA binding.

Localization (import) of Smad3 associated with repression

2) Confidence 0.54 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2682659 Disease Relevance 0.27 Pain Relevance 0

However, none of the Sox17 proteins influenced nuclear translocation of Smad3 in the presence or absence of TGF-?

Localization (translocation) of Smad3

3) Confidence 0.51 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2682659 Disease Relevance 0.22 Pain Relevance 0

Genes monitored were smad2, smad3, TGF-?

Localization (were) of smad3

4) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2659748 Disease Relevance 0.27 Pain Relevance 0

Primer pairs (Invitrogen) used were smad2 (For: CGGAGATTCTAACAGAACTG; Rev: TGCTTGAGCATCGCACTGAA), smad3 (For: AGCACACAATAACTTGGACC; Rev: TAAGACACACTGGAACAGCGGATG), TGF-?

Localization (were) of smad3

5) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2659748 Disease Relevance 0.20 Pain Relevance 0

The phosphorylated Smad2 and Smad3 then form a complex with Smad4 and translocate to the nucleus [29,30].

Localization (translocate) of Smad3 in nucleus

6) Confidence 0.38 Published 2010 Journal Molecular Vision Section Body Doc Link PMC3013068 Disease Relevance 0.08 Pain Relevance 0.04

General Comments

This test has worked.