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Context Info
Confidence 0.13
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 1.31
Pain Relevance 0.03

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

signal transduction (IGF1, CREB1) nucleoplasm (CREB1) mitochondrion (CREB1)
extracellular space (IGF1) extracellular region (IGF1) nucleolus (CREB1)
Anatomy Link Frequency
neurons 1
IGF1 (Homo sapiens)
CREB1 (Homo sapiens)
Pain Link Frequency Relevance Heat
ischemia 1 50.28 Quite High
Inflammatory marker 4 50.00 Quite Low
Central nervous system 1 46.84 Quite Low
projection neuron 1 6.48 Low Low
Inflammation 4 5.00 Very Low Very Low Very Low
cytokine 2 5.00 Very Low Very Low Very Low
imagery 2 5.00 Very Low Very Low Very Low
carpal tunnel syndrome 1 5.00 Very Low Very Low Very Low
rheumatoid arthritis 1 5.00 Very Low Very Low Very Low
Serotonin 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 8 100.00 Very High Very High Very High
Death 6 93.16 High High
Obesity 7 86.96 High High
Aging 4 65.68 Quite High
Atherosclerosis 12 65.12 Quite High
Cerebrovascular Disease 3 63.52 Quite High
Cognitive Disorder 2 61.52 Quite High
Dementia 2 59.68 Quite High
Cardiovascular Disease 12 51.12 Quite High
Cv General 4 Under Development 1 50.28 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
High glucose also induces loss of the initiator caspase-9 and increases caspase-3 cleavage, effects blocked by IGF-I, suggesting that IGF-I prevents apoptosis in DRG neurons by regulating PI3K/Akt pathway effectors, including GSK-3beta, CREB, and FKHR, and by blocking caspase activation (Leinninger et al 2004).
IGF-I Regulation (regulating) of CREB in neurons associated with apoptosis
1) Confidence 0.13 Published 2008 Journal Vascular Health and Risk Management Section Body Doc Link PMC2663454 Disease Relevance 1.31 Pain Relevance 0.03

General Comments

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