INT303334

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Context Info
Confidence 0.00
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 0.11
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.

cell differentiation (Grb2) endosome (Grb2) anatomical structure formation involved in morphogenesis (Grb2)
aging (Grb2) Golgi apparatus (Grb2) intracellular (SOS1)
Anatomy Link Frequency
SH3 1
SOS1 (Homo sapiens)
Grb2 (Mus musculus)
Pain Link Frequency Relevance Heat
Spinal cord 14 5.00 Very Low Very Low Very Low
medulla 8 5.00 Very Low Very Low Very Low
midbrain 4 5.00 Very Low Very Low Very Low
withdrawal 4 5.00 Very Low Very Low Very Low
Hippocampus 4 5.00 Very Low Very Low Very Low
cytokine 2 5.00 Very Low Very Low Very Low
backache 2 5.00 Very Low Very Low Very Low
Kinase C 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Repression 6 58.40 Quite High
Motor Neuron Diseases 124 50.00 Quite Low
Stress 6 35.20 Quite Low
Dementia 30 5.00 Very Low Very Low Very Low
Disease 26 5.00 Very Low Very Low Very Low
Neurodegenerative Disease 16 5.00 Very Low Very Low Very Low
Spinal Muscular Atrophy 14 5.00 Very Low Very Low Very Low
Injury 8 5.00 Very Low Very Low Very Low
Apoptosis 8 5.00 Very Low Very Low Very Low
Fasciculation 8 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Once bound by GRB2, SOS catalyses the substitution of GDP to GTP on RAS (?
SOS Binding (bound) of GRB2
1) Confidence 0.00 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844426 Disease Relevance 0.06 Pain Relevance 0
The phosphorylated tyrosine of the target protein is bound by the SH2 domain of GRB2, which also contains an SH3 domain that binds to the proline-rich region of SOS.
SOS Binding (binds) of GRB2 in SH3
2) Confidence 0.00 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844426 Disease Relevance 0.06 Pain Relevance 0

General Comments

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