INT309158

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Context Info
Confidence 0.04
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 1.39
Pain Relevance 0.61

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

mitochondrion (Dlat) transferase activity, transferring acyl groups (Dlat) enzyme binding (Esr1)
DNA binding (Esr1) protein complex (Esr1) cytoplasm (Esr1)
Anatomy Link Frequency
brain 1
nucleus 1
Esr1 (Mus musculus)
Dlat (Rattus norvegicus)
Pain Link Frequency Relevance Heat
ischemia 134 87.92 High High
agonist 4 87.48 High High
Hippocampus 28 72.08 Quite High
antagonist 16 68.72 Quite High
bDMF 48 64.08 Quite High
anesthesia 8 5.00 Very Low Very Low Very Low
cerebral cortex 2 5.00 Very Low Very Low Very Low
Pyramidal cell 2 5.00 Very Low Very Low Very Low
halothane 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Cv General 4 Under Development 118 87.92 High High
Apoptosis 10 87.92 High High
Middle Cerebral Artery Infarction 6 83.28 Quite High
Cv Unclassified Under Development 12 82.00 Quite High
Targeted Disruption 18 76.24 Quite High
Death 12 67.20 Quite High
Cognitive Disorder 32 53.68 Quite High
Endometriosis (extended) 4 48.48 Quite Low
Stroke 12 45.12 Quite Low
Disease 4 21.56 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
It has been predominantly thought that E2 neuroprotection in the brain is mediated principally by the “classical” nuclear ER-mediated genomic signaling pathway, which involves E2 interaction with nuclear ER and regulation of transcription of various genes that mediate neuroprotection.
nuclear ER Binding (interaction) of E2 in brain
1) Confidence 0.04 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866326 Disease Relevance 1.06 Pain Relevance 0.37
EDC and E2-BSA retain their ability to induce rapid extranuclear-mediated nongenomic signaling, but lack significant nuclear ER-mediated genomic signaling ability due to their inability to enter the cell nucleus and interact with nuclear ER [32], [33].
nuclear ER Binding (interact) of E2 in nucleus
2) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866326 Disease Relevance 0.34 Pain Relevance 0.24

General Comments

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