INT187346

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Context Info
Confidence 0.29
First Reported 2005
Last Reported 2010
Negated 1
Speculated 1
Reported most in Body
Documents 12
Total Number 13
Disease Relevance 1.82
Pain Relevance 4.28

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

mitochondrion (Dlat) transferase activity, transferring acyl groups (Dlat)
Anatomy Link Frequency
neuronal 1
plasma 1
neurons 1
medial 1
brain 1
Dlat (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Dopamine 41 99.84 Very High Very High Very High
antagonist 22 99.38 Very High Very High Very High
Somatostatin 628 99.26 Very High Very High Very High
Hippocampus 65 98.26 Very High Very High Very High
ischemia 175 97.88 Very High Very High Very High
spinal dorsal horn 51 97.52 Very High Very High Very High
Pyramidal cell 51 95.20 Very High Very High Very High
Glutamate 2 94.96 High High
bDMF 24 90.72 High High
agonist 40 88.36 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 19 99.16 Very High Very High Very High
Cv General 4 Under Development 61 97.88 Very High Very High Very High
Cv Unclassified Under Development 110 87.96 High High
Death 20 83.76 Quite High
Stress 5 80.64 Quite High
Pain 15 77.72 Quite High
Nociception 12 72.96 Quite High
Aging 8 54.28 Quite High
Reprotox - General 1 10 49.52 Quite Low
Thrombosis 4 48.80 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To explore whether a genomic mechanism is responsible for E2 inhibition on IGly, we first examined the effect of E2 in large outside-out patches excised from cultured HIP neurons.
Spec (whether) Regulation (responsible) of E2 in neurons
1) Confidence 0.29 Published 2009 Journal Mol Pain Section Body Doc Link PMC2651124 Disease Relevance 0 Pain Relevance 0.06
GPR30 is widely expressed in the brain including the hippocampus [14], and a recent study with GPR30 knockout mice shows that GPR30 is not involved in E2 regulation of female reproductive functions known to be mediated by ER?
Regulation (regulation) of E2 in brain associated with targeted disruption and hippocampus
2) Confidence 0.24 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2799530 Disease Relevance 0.43 Pain Relevance 0.29
We suggest that the neuronal GlyR is a novel molecular target of E2 which directly inhibits the function of GlyRs in the HIP and SDH regions.
Regulation (target) of E2 in neuronal associated with spinal dorsal horn
3) Confidence 0.17 Published 2009 Journal Mol Pain Section Abstract Doc Link PMC2651124 Disease Relevance 0.06 Pain Relevance 0.24
Second, it is unlikely that E2 physically disrupts the plasma membrane via a nonspecific way as E2 only affected ?
Regulation (affected) of E2 in plasma
4) Confidence 0.15 Published 2009 Journal Mol Pain Section Body Doc Link PMC2651124 Disease Relevance 0.15 Pain Relevance 0.15
These data suggest that the number of SOM-ir cells in the female PeVN is also dependent on OVX length rather than on E2 treatment alone.
Regulation (dependent) of E2 associated with somatostatin
5) Confidence 0.14 Published 2008 Journal Exp Brain Res Section Body Doc Link PMC2441535 Disease Relevance 0 Pain Relevance 0.54
E2 or P treatment alone affected neither the total number of SOM-ir cells nor the total SOM-ir area in the PeVN (Fig. 5a, b).
Neg (neither) Regulation (affected) of E2 associated with somatostatin
6) Confidence 0.14 Published 2008 Journal Exp Brain Res Section Body Doc Link PMC2441535 Disease Relevance 0 Pain Relevance 0.72
, was originally shown to mimic E2 modulation of hypothalamic ion channels and phospholipase C through the activation of a G-protein coupled receptor (for review see [10]).
Regulation (modulation) of E2
7) Confidence 0.12 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2799530 Disease Relevance 0.37 Pain Relevance 0.32
Thus, E2 dependent down regulation of epithelial cells in the uterus would be at least partly ER?
Regulation (regulation) of E2 in epithelial cells
8) Confidence 0.10 Published 2006 Journal Reprod Biol Endocrinol Section Body Doc Link PMC1586009 Disease Relevance 0.27 Pain Relevance 0
This effect of combined E2 and P on the number of SOM-ir cells and on the SOM-ir area was most pronounced in the medial and posterior parts of the PeVN, although the differences in each sub-region did not reach statistical significance (data not shown).


Regulation (effect) of E2 in posterior associated with somatostatin
9) Confidence 0.09 Published 2008 Journal Exp Brain Res Section Body Doc Link PMC2441535 Disease Relevance 0 Pain Relevance 0.68
The latency to the first penile reflex and the frequency of E2 and E3 responses were not significantly different.
Regulation (responses) of E2
10) Confidence 0.07 Published 2005 Journal Environ Health Perspect Section Body Doc Link PMC1257594 Disease Relevance 0 Pain Relevance 0
Furthermore, as shown in Fig. 6, additional work suggests that EDC and E2-BSA regulatory effects upon ERK, Akt and JNK activation after GCI are mediated by estrogen receptors, as pretreatment with the ER antagonist, ICI182,780 abolished EDC and E2-BSA modulation of ERK, Akt and JNK activation in the CA1 region at 10min reperfusion.


Regulation (modulation) of E2 associated with antagonist and ischemia
11) Confidence 0.04 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2866326 Disease Relevance 0.54 Pain Relevance 0.41
This effect of combined E2 and P on the number of SOM-ir cells and on the SOM-ir area was most pronounced in the medial and posterior parts of the PeVN, although the differences in each sub-region did not reach statistical significance (data not shown).


Regulation (effect) of E2 in medial associated with somatostatin
12) Confidence 0.03 Published 2008 Journal Exp Brain Res Section Body Doc Link PMC2441535 Disease Relevance 0 Pain Relevance 0.68
We next addressed the affect of 10 nM E2 on DA uptake.
Regulation (affect) of E2 associated with dopamine
13) Confidence 0.03 Published 2006 Journal J Mol Signal Section Body Doc Link PMC1769494 Disease Relevance 0 Pain Relevance 0.18

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