INT348524

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Context Info
Confidence 0.07
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 3
Disease Relevance 0.59
Pain Relevance 0

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

nucleus (FOSL2, JUN) nucleoplasm (JUN) nuclear chromosome (JUN)
aging (JUN) DNA binding (JUN) cytosol (JUN)
FOSL2 (Homo sapiens)
JUN (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 9 5.00 Very Low Very Low Very Low
cytokine 6 5.00 Very Low Very Low Very Low
alcohol 3 5.00 Very Low Very Low Very Low
abdominal pain 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 408 99.20 Very High Very High Very High
Cancer 24 76.24 Quite High
Infection 78 33.28 Quite Low
Cervical Cancer 3 7.92 Low Low
Papillomavirus Infection 3 5.60 Low Low
Death 18 5.00 Very Low Very Low Very Low
Repression 12 5.00 Very Low Very Low Very Low
Sprains And Strains 12 5.00 Very Low Very Low Very Low
Retinoblastoma 9 5.00 Very Low Very Low Very Low
Necrosis 9 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
FOSL2 is a part of the AP-1 transcription factor complex and has been shown to dimerize with JUN [46].
FOSL2 Binding (dimerize) of JUN
1) Confidence 0.07 Published 2010 Journal BMC Genomics Section Body Doc Link PMC2996966 Disease Relevance 0.14 Pain Relevance 0
This induction may be a result of the high induction levels of the genes associated with AP-1 complexes, namely JUN, JUND, and FOSL2.
FOSL2 Binding (complexes) of AP-1
2) Confidence 0.06 Published 2010 Journal BMC Genomics Section Body Doc Link PMC2996966 Disease Relevance 0.32 Pain Relevance 0
FOSL2 is a part of the AP-1 transcription factor complex and has been shown to dimerize with JUN [46].
FOSL2 Binding (dimerize) of AP-1
3) Confidence 0.06 Published 2010 Journal BMC Genomics Section Body Doc Link PMC2996966 Disease Relevance 0.14 Pain Relevance 0

General Comments

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