INT149795

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Context Info
Confidence 0.73
First Reported 2005
Last Reported 2011
Negated 0
Speculated 1
Reported most in Body
Documents 8
Total Number 12
Disease Relevance 1.50
Pain Relevance 3.06

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

lyase activity (Ddc) cellular amino acid metabolic process (Ddc) cytoplasm (Ddc)
Anatomy Link Frequency
Pet1 3
dorsal 1
glial cell 1
neurons 1
striatum 1
Ddc (Mus musculus)
Pain Link Frequency Relevance Heat
Dopamine 529 100.00 Very High Very High Very High
Raphe 80 98.20 Very High Very High Very High
monoamine 53 97.04 Very High Very High Very High
Neurotransmitter 23 96.04 Very High Very High Very High
Serotonin 23 95.32 Very High Very High Very High
Enkephalin 2 93.08 High High
Dynorphin 2 92.48 High High
Nucleus accumbens 4 87.80 High High
Ventral tegmentum 18 84.56 Quite High
Substantia nigra 30 78.04 Quite High
Disease Link Frequency Relevance Heat
Parkinson's Disease 169 92.08 High High
Schizophrenia 5 91.16 High High
Dyskinesias 18 90.44 High High
Disease 109 89.96 High High
Aging 15 86.28 High High
Body Weight 16 80.76 Quite High
Congenital Anomalies 9 67.48 Quite High
Neurodegenerative Disease 12 57.76 Quite High
Targeted Disruption 23 56.60 Quite High
Tremor 23 48.44 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To test whether deleting Lmx1b decreases the number of 5-HTergic neurons or not, which in turn results in the phenotypes mentioned above, we examined the expression of Aadc and Pet1.
Spec (examined) Gene_expression (expression) of Aadc in Pet1
1) Confidence 0.73 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3016403 Disease Relevance 0 Pain Relevance 0.11
In contrast, the expression of both Pet1 and Aadc appeared unchanged in Lmx1b iCKO mice relative to control mice, indicating that there was no loss of 5-HTergic neurons in the raphe nuclei.
Gene_expression (expression) of Aadc in neurons associated with raphe
2) Confidence 0.73 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3016403 Disease Relevance 0 Pain Relevance 0.13
On the other hand, the expression of dopamine and norepinephrine as well as aromatic L-amino acid decarboxylase (Aadc) and Pet1 was unchanged.
Gene_expression (expression) of Aadc in Pet1 associated with dopamine
3) Confidence 0.56 Published 2011 Journal PLoS ONE Section Abstract Doc Link PMC3016403 Disease Relevance 0 Pain Relevance 0.26
In situ hybridization probes against Tph2, Sert, Aadc and Dopamine ?
Gene_expression (probes) of Aadc associated with dopamine
4) Confidence 0.55 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3016403 Disease Relevance 0.20 Pain Relevance 0.05
On the other hand, the expression of dopamine and norepinephrine as well as aromatic L-amino acid decarboxylase (Aadc) and Pet1 was unchanged.
Gene_expression (expression) of L-amino acid decarboxylase in Pet1 associated with dopamine
5) Confidence 0.49 Published 2011 Journal PLoS ONE Section Abstract Doc Link PMC3016403 Disease Relevance 0 Pain Relevance 0.26
DA is synthesized from tyrosine by the rate-limiting enzyme tyrosine hydroxylase (TH), to produce L-DOPA which is quickly decarboxylated by L-aromatic acid decarboxylase (L-AADC) to DA [1,3].
Gene_expression (produce) of L-DOPA associated with dopamine
6) Confidence 0.48 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1181539 Disease Relevance 0.07 Pain Relevance 0.87
TH-ir neurones did not express the dopamine transporter but half of them expressed amino acid decarboxylase, an enzyme required for dopamine synthesis.
Gene_expression (expressed) of amino acid decarboxylase associated with dopamine
7) Confidence 0.39 Published 2008 Journal Eur. J. Neurosci. Section Abstract Doc Link 18279311 Disease Relevance 0.05 Pain Relevance 0.31
At the same time, a second treatment 2 h later by the same dose of the drug failed to induce locomotion in DD mice suggesting that this effect is dependent upon residual (after L-DOPA administration) DA which might be depleted by the first treatment with the drug [76].
Gene_expression (administration) of L-DOPA associated with dopamine
8) Confidence 0.36 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1181539 Disease Relevance 0 Pain Relevance 0.48
Although there is extensive evidence for TH-ir neurones in the lesioned rodent striatum, there are few details regarding the molecular phenotype of these neurones, regulation of their TH expression after l-3,4-dihydroxyphenylalanine (L-DOPA) treatment and their function.
Gene_expression (expression) of L-DOPA in striatum
9) Confidence 0.26 Published 2008 Journal Eur. J. Neurosci. Section Abstract Doc Link 18279311 Disease Relevance 0.09 Pain Relevance 0.08
During DA synthesis, L-DOPA is produced from the amino acid tyrosine by tyrosine hydroxylase (TH) and further decarboxylated by L-aromatic acid decarboxylase (L-AADC) to yield DA [1], [2].
Gene_expression (produced) of L-DOPA associated with dopamine
10) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2956650 Disease Relevance 0.27 Pain Relevance 0.32
Some of the gene therapies attempted to date include glial cell line-derived neurotrophic factor (GDNF) and enzymes involved in dopamine synthesis (tyrosine hydroxylase (TH) and aromatic acid decarboxylase (AADC)) with limited success [12, 13].
Gene_expression (synthesis) of aromatic acid decarboxylase in glial cell associated with dopamine
11) Confidence 0.09 Published 2011 Journal Parkinson's Disease Section Body Doc Link PMC3005838 Disease Relevance 0.28 Pain Relevance 0.09
One is characterized by DOPA decarboxylase decrease involving both the nigrostriatal and the mesolimbic compartments, and is responsible for the moderate DA decrease in the dorsal striatum.
Gene_expression (decrease) of DOPA decarboxylase in dorsal
12) Confidence 0.07 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2978035 Disease Relevance 0.54 Pain Relevance 0.09

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