INT28458

From wiki-pain
Revision as of 15:49, 24 September 2012 by Daniel (Talk | contribs)

(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Jump to: navigation, search
Context Info
Confidence 0.76
First Reported 1989
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 31
Total Number 32
Disease Relevance 2.33
Pain Relevance 12.49

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
nucleus accumbens 5
plasma 4
striatum 4
vesicles 3
DA neurons 1
Slc6a3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Dopamine 1170 100.00 Very High Very High Very High
opioid receptor 9 100.00 Very High Very High Very High
Morphine 28 99.84 Very High Very High Very High
Nucleus accumbens 39 99.68 Very High Very High Very High
Catechol-O-methyltransferase 1 99.46 Very High Very High Very High
Nicotine 28 99.44 Very High Very High Very High
midbrain 10 98.64 Very High Very High Very High
Serotonin 29 98.50 Very High Very High Very High
dopamine receptor 1 98.24 Very High Very High Very High
opiate 4 98.00 Very High Very High Very High
Disease Link Frequency Relevance Heat
Depression 66 99.34 Very High Very High Very High
Hyperglycemia 5 97.56 Very High Very High Very High
Congenital Anomalies 9 96.44 Very High Very High Very High
Drug Dependence 35 93.16 High High
Alcohol Addiction 33 91.52 High High
Stress 46 85.20 High High
Disease 81 84.40 Quite High
Death 13 83.92 Quite High
Post-partum Depression 5 75.04 Quite High
Alcoholic Liver Diseases 41 73.92 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Localization of the delta-opioid receptor and dopamine transporter in the nucleus accumbens shell: implications for opiate and psychostimulant cross-sensitization.
Localization (Localization) of dopamine transporter in nucleus accumbens associated with nucleus accumbens, dopamine, opiate and opioid receptor
1) Confidence 0.76 Published 1999 Journal Synapse Section Title Doc Link 10459166 Disease Relevance 0 Pain Relevance 0.78
However, coexpression of the MG encoding the peptide DAT-CT583–620 significantly inhibited the increasing effects of DAT-mediated DA translocation by CPE.
Localization (translocation) of DAT-mediated associated with dopamine
2) Confidence 0.66 Published 2009 Journal Mol Brain Section Body Doc Link PMC2687442 Disease Relevance 0 Pain Relevance 0.25
Immunoprecipitation of DAT was carried out.


Localization (Immunoprecipitation) of DAT
3) Confidence 0.66 Published 2009 Journal Mol Brain Section Body Doc Link PMC2687442 Disease Relevance 0 Pain Relevance 0.05
To directly examine the cellular effects of CPE on DAT, we analyzed subcellular localization of DAT and CPE in transfected HEK-293 cells using confocal immunofluorescence microscopy.
Spec (analyzed) Localization (localization) of DAT
4) Confidence 0.66 Published 2009 Journal Mol Brain Section Body Doc Link PMC2687442 Disease Relevance 0 Pain Relevance 0.14
Also, both ultrastructural and biochemical studies revealed the localization of DAT in endosomes and tubulo-vesicular membranes but not biosynthetic machinery, suggesting that most of intracellular DAT- positive vesicles are endocytic but not secretory [14,37].
Localization (localization) of DAT in vesicles
5) Confidence 0.66 Published 2009 Journal Mol Brain Section Body Doc Link PMC2687442 Disease Relevance 0 Pain Relevance 0.12
Conversely, Hic-5, a LIM domain containing protein, has also been shown to bind to the DAT-CT and inhibit DAT localization to the plasma membrane [17].
Localization (localization) of DAT in plasma
6) Confidence 0.66 Published 2009 Journal Mol Brain Section Body Doc Link PMC2687442 Disease Relevance 0.24 Pain Relevance 0.04
We have shown that this interaction leads to cell surface stabilization of DAT via reduced degradation, possibly through a reduction in DAT phosphorylation.
Localization (stabilization) of DAT
7) Confidence 0.62 Published 2009 Journal Mol Brain Section Body Doc Link PMC2687442 Disease Relevance 0 Pain Relevance 0.18
In virtually all cells coexpressing DAT and CPE, DAT was largely found at the plasma membrane and colocalized with CPE (Fig. 3C).
Localization (colocalized) of DAT in plasma
8) Confidence 0.62 Published 2009 Journal Mol Brain Section Body Doc Link PMC2687442 Disease Relevance 0 Pain Relevance 0.03
In addition, CPE association could reduce the phosphorylation state of DAT on serine residues, potentially leading to reduced internalization, thus stabilizing plasmalemmal DAT localization.


Localization (localization) of DAT
9) Confidence 0.58 Published 2009 Journal Mol Brain Section Abstract Doc Link PMC2687442 Disease Relevance 0 Pain Relevance 0.14
Therefore, it is conceivable that PI3K signaling and ultimately Akt, by fine-tuning DAT expression at the plasma membrane [13,29], regulate the ability of AMPH to cause DAT-mediated DA efflux.
Localization (cause) of DAT-mediated in plasma associated with dopamine
10) Confidence 0.53 Published 2007 Journal PLoS Biology Section Body Doc Link PMC2020502 Disease Relevance 0 Pain Relevance 0.32
Thus, at doses of 30 micrograms/kg s.c., ICS 205-930 completely prevented the morphine-, nicotine- and ethanol-induced stimulation of DA release in the nucleus accumbens; doses of 15 micrograms/kg s.c. partially prevented the morphine-, nicotine- and ethanol-induced stimulation of DA release while doses of 7.5 micrograms/kg s.c. were ineffective.
Localization (release) of DA in nucleus accumbens associated with nucleus accumbens, dopamine, nicotine and morphine
11) Confidence 0.53 Published 1989 Journal Eur. J. Pharmacol. Section Abstract Doc Link 2767122 Disease Relevance 0 Pain Relevance 1.16
In contrast, ICS 205-930 (up to 30 micrograms/kg s.c.) failed to affect the amphetamine-induced stimulation of DA release in the nucleus accumbens.
Localization (release) of DA in nucleus accumbens associated with nucleus accumbens and dopamine
12) Confidence 0.53 Published 1989 Journal Eur. J. Pharmacol. Section Abstract Doc Link 2767122 Disease Relevance 0 Pain Relevance 1.15
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.
Localization (localization) of DAT
13) Confidence 0.51 Published 2009 Journal Mol Brain Section Abstract Doc Link PMC2687442 Disease Relevance 0 Pain Relevance 0.15
In addition, CPE association could reduce the phosphorylation state of DAT on serine residues, potentially leading to reduced internalization, thus stabilizing plasmalemmal DAT localization.


Localization (localization) of DAT
14) Confidence 0.51 Published 2009 Journal Mol Brain Section Abstract Doc Link PMC2687442 Disease Relevance 0 Pain Relevance 0.14
Once DA is released into the synapse, the DA transporter (DAT) is the primary mechanism for clearing the transmitter from the extracellular space, particularly within the striatum [3–5].
Localization (released) of DAT in striatum associated with dopamine
15) Confidence 0.50 Published 2007 Journal PLoS Biology Section Body Doc Link PMC2020502 Disease Relevance 0.30 Pain Relevance 0.40
Once DA is released into the synapse, the DA transporter (DAT) is the primary mechanism for clearing the transmitter from the extracellular space, particularly within the striatum [3–5].
Localization (released) of DA transporter in striatum associated with dopamine
16) Confidence 0.50 Published 2007 Journal PLoS Biology Section Body Doc Link PMC2020502 Disease Relevance 0.30 Pain Relevance 0.40
Here we show that pharmacological manipulation of the PI3K signaling pathway caused by hypoinsulinemic conditions or selective pharmacological inhibition/activation of PI3K dramatically regulates the ability of AMPH to evoke DAT-mediated DA release in the striatum, as determined by HSCA.
Localization (release) of DAT-mediated in striatum associated with dopamine
17) Confidence 0.50 Published 2007 Journal PLoS Biology Section Body Doc Link PMC2020502 Disease Relevance 0.07 Pain Relevance 0.28
Because hyperglycemia has been shown to not significantly influence BOLD signals [66], our data suggest that blunting of the AMPH-induced BOLD response in the DAT-dense striatum of insulin-depleted rats (Figure 5) is not due to STZ-mediated metabolic abnormalities.
Localization (response) of DAT in striatum associated with hyperglycemia and congenital anomalies
18) Confidence 0.46 Published 2007 Journal PLoS Biology Section Body Doc Link PMC2020502 Disease Relevance 0.19 Pain Relevance 0.22
The inhibitory effects of ICS 205-930 (15 and 30 micrograms/kg s.c.) on the drug-induced stimulation of DA release could also be extended to the neuroleptic haloperidol (0.1 mg/kg s.c.).
Localization (release) of DA associated with dopamine
19) Confidence 0.46 Published 1989 Journal Eur. J. Pharmacol. Section Abstract Doc Link 2767122 Disease Relevance 0 Pain Relevance 1.10
Thus, at doses of 30 micrograms/kg s.c., ICS 205-930 completely prevented the morphine-, nicotine- and ethanol-induced stimulation of DA release in the nucleus accumbens; doses of 15 micrograms/kg s.c. partially prevented the morphine-, nicotine- and ethanol-induced stimulation of DA release while doses of 7.5 micrograms/kg s.c. were ineffective.
Localization (release) of DA in nucleus accumbens associated with nucleus accumbens, dopamine, nicotine and morphine
20) Confidence 0.46 Published 1989 Journal Eur. J. Pharmacol. Section Abstract Doc Link 2767122 Disease Relevance 0 Pain Relevance 1.20

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox