INT228249

Context Info Confidence 0.48 First Reported 2008 Last Reported 2011 Negated 0 Speculated 0 Reported most in Body Documents 7 Total Number 7 Disease Relevance 3.26 Pain Relevance 1.45

phosphatase activity (Pten) mitochondrion (Pten) plasma membrane (Pten) nucleus (Pten) intracellular (Pten) enzyme binding (Pten)

Anatomy Link Frequency neuronal 1 midbrain 1 oligodendrocyte 1 Pten (Mus musculus)

Pain Link Frequency Relevance Heat midbrain 60 97.24 Glutamate 4 97.04 Serotonin 12 96.48 agonist 22 96.20 Dopamine 460 94.08 Ventral tegmentum 32 92.04 Substantia nigra 32 91.72 Hippocampus 5 90.32 cerebral cortex 4 89.68 Nicotine 4 66.48

Disease Link Frequency Relevance Heat Apoptosis 68 95.60 Cancer 150 94.00 Congenital Anomalies 4 93.52 Glioma 49 93.20 Hypertrophy 12 92.44 Macrocephaly 8 91.32 Adenocarcinoma 60 89.80 Death 39 87.00 Disease 24 81.44 Targeted Disruption 38 78.48

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

Besides the inhibitory control on the activation of the Akt pathway, PTEN interacts with molecular substrates directly involved in neurotransmission such as glutamate and serotonin receptors [13], [14].

PTEN Binding (interacts) of associated with glutamate and serotonin

1) Confidence 0.48 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2736587 Disease Relevance 0.43 Pain Relevance 0.60

Recent studies have emphasized the association of PTEN with different parameters of the dopaminergic system in the ventral midbrain.

PTEN Binding (association) of in midbrain associated with midbrain

2) Confidence 0.48 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2736587 Disease Relevance 0.57 Pain Relevance 0.32

A common phenotype associated with the loss of PTEN in neuronal populations is an enlargement of neuronal soma size, increased cell proliferation, inhibition of apoptosis, and the expression of thickened axonal and dendritic processes.

PTEN Binding (loss) of in neuronal associated with apoptosis

3) Confidence 0.37 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2736587 Disease Relevance 0.17 Pain Relevance 0.40

Sections were incubated with a mouse monoclonal anti PTEN (Cell Signaling, Danvers, MA) or with anti p-AKT rabbit monoclonal antibody (1?

PTEN Binding (incubated) of

4) Confidence 0.37 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2736587 Disease Relevance 0 Pain Relevance 0.05

Recently, by the help of high-throughput genome and transcriptome analyses, human secondary GBs were shown to be similar to the proneural type of primary GBs and associated with PDGFRA amplification, TP53 and PTEN deletion/mutation, IDH1 mutation and also disturbances in the PI3K signaling pathway, and finally by the expression of oligodendrocyte markers [133].

PTEN Binding (associated) of in oligodendrocyte

5) Confidence 0.29 Published 2011 Journal Journal of Oncology Section Body Doc Link PMC3010739 Disease Relevance 0.76 Pain Relevance 0

This agrees with the reduction of PTEN

PTEN Binding (agrees) of

6) Confidence 0.22 Published 2008 Journal PPAR Research Section Body Doc Link PMC2430014 Disease Relevance 0.62 Pain Relevance 0.08

Our results further suggest that PKB activity lacked significant association with its antagonistic regulator PTEN as well as with downstream PKB substrates including GSK3?

PTEN Binding (association) of

7) Confidence 0.14 Published 2008 Journal BMC Cancer Section Body Doc Link PMC2270852 Disease Relevance 0.72 Pain Relevance 0

General Comments

This test has worked.