INT77990

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.72
First Reported 1998
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 6
Disease Relevance 0.99
Pain Relevance 1.84

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

aging (Slc6a3) plasma membrane (Slc6a3) transmembrane transport (Slc6a3)
Anatomy Link Frequency
neuronal 1
Slc6a3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Dopamine 177 100.00 Very High Very High Very High
monoamine 4 99.36 Very High Very High Very High
cocaine 5 98.52 Very High Very High Very High
withdrawal 4 92.96 High High
MU agonist 3 92.88 High High
agonist 1 91.52 High High
Eae 1 90.52 High High
Kinase C 45 84.64 Quite High
Nucleus accumbens 6 80.68 Quite High
Hippocampus 2 61.96 Quite High
Disease Link Frequency Relevance Heat
Hypoxia 64 89.20 High High
Stress 32 87.64 High High
Shock 1 81.28 Quite High
Learning Disorders 2 76.52 Quite High
Congenital Anomalies 2 75.48 Quite High
Death 5 67.08 Quite High
Heart Rate Under Development 38 54.56 Quite High
Hypertension 9 50.00 Quite Low
Hypocapnia 3 46.76 Quite Low
Disease 15 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Cell surface expression and degradation of DAT [31] is modulated by various cellular signals, substrates and neuronal activity.
Protein_catabolism (degradation) of DAT in neuronal
1) Confidence 0.72 Published 2009 Journal Mol Brain Section Body Doc Link PMC2687442 Disease Relevance 0 Pain Relevance 0.08
These data suggested that CPE modulated DAT via a posttranslational mechanism, which possibly included reduced degradation of surface DAT.
Protein_catabolism (degradation) of DAT
2) Confidence 0.72 Published 2009 Journal Mol Brain Section Body Doc Link PMC2687442 Disease Relevance 0 Pain Relevance 0
Functional changes caused by CPE could be attributed to enhanced DAT expression and subsequent increase in DAT cell surface localization, due to decreased DAT degradation.
Protein_catabolism (degradation) of DAT
3) Confidence 0.47 Published 2009 Journal Mol Brain Section Abstract Doc Link PMC2687442 Disease Relevance 0 Pain Relevance 0.15
There were no differences in either the total amount of dopamine taken up or in the IC50 for cocaine to inhibit dopamine uptake following this treatment, suggesting that the dopamine transporter and presynaptic terminals were intact.
Protein_catabolism (intact) of dopamine transporter associated with dopamine and cocaine
4) Confidence 0.43 Published 1998 Journal Synapse Section Abstract Doc Link 9776131 Disease Relevance 0 Pain Relevance 0.91
Next we looked at the whole-cell levels of DAT protein, to determine if E2 might have an effect on rapid DAT protein stability.
Protein_catabolism (stability) of DAT protein
5) Confidence 0.32 Published 2006 Journal J Mol Signal Section Body Doc Link PMC1769494 Disease Relevance 0 Pain Relevance 0
Instead, it is thought that the increased DA levels were mainly caused by persistence of DA due to decreased reuptake resulting from weakening of DA transporter activity (Nakajima et al., 1996; Orset et al., 2005) and decreased degradation due to lowered monoamine oxidase activity (Nakajima et al., 1996).
Protein_catabolism (degradation) of DA transporter associated with dopamine and monoamine
6) Confidence 0.22 Published 2008 Journal Autonomic Neuroscience Section Body Doc Link PMC2941824 Disease Relevance 0.99 Pain Relevance 0.71

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox