INT200872

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Context Info
Confidence 0.22
First Reported 2006
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 16
Total Number 18
Disease Relevance 5.61
Pain Relevance 3.30

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

transport (Gopc) Golgi apparatus (Gopc) plasma membrane (Gopc)
cytoplasm (Gopc)
Anatomy Link Frequency
muscle 4
hearts 2
synapses 2
interneurons 2
cardiomyocytes 1
Gopc (Mus musculus)
Pain Link Frequency Relevance Heat
Dopamine 115 100.00 Very High Very High Very High
metalloproteinase 93 100.00 Very High Very High Very High
depression 26 100.00 Very High Very High Very High
Neurotransmitter 18 100.00 Very High Very High Very High
GABAergic 13 100.00 Very High Very High Very High
Glutamate 12 100.00 Very High Very High Very High
antagonist 115 98.12 Very High Very High Very High
cytokine 60 96.04 Very High Very High Very High
Hippocampus 38 95.84 Very High Very High Very High
Inflammation 65 95.64 Very High Very High Very High
Disease Link Frequency Relevance Heat
Cancer 525 100.00 Very High Very High Very High
Depression 26 100.00 Very High Very High Very High
Diabetes Mellitus 154 99.84 Very High Very High Very High
Targeted Disruption 144 99.06 Very High Very High Very High
INFLAMMATION 72 95.64 Very High Very High Very High
Immunization 10 90.16 High High
Apoptosis 43 89.20 High High
Death 28 85.92 High High
Severe Combined Immunodeficiency 32 84.16 Quite High
Fatigue 17 75.72 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Collectively, these results demonstrate that a lack of dysbindin leads to larger but fewer glutamatergic vesicles, narrower synaptic clefts, and thicker PSDs within CA1 asymmetrical synapses, in agreement with our electrophysiological observations of slow dynamics and reduced probability of glutamate release (Fig. 4).


Negative_regulation (reduced) of Localization (probability) of Fig in synapses associated with glutamate
1) Confidence 0.22 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2396815 Disease Relevance 0 Pain Relevance 0.18
Moreover, both secretion of NSE (Fig. 6D, left panel) and CgA accumulation (Fig. 6D, right panel and Figure S1) were markedly diminished while Akt phosphorylation was unchanged hence suggesting that SphK1 inhibition can to a certain extent block the NE transdifferentiation.
Negative_regulation (diminished) of Localization (secretion) of Fig
2) Confidence 0.19 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2779655 Disease Relevance 0 Pain Relevance 0
This indicates that CAR KO cardiomyocytes, unlike AV nodal cells are not limited by GAP junction activity, a feature which could derive both from altered expression of connexins and differential localization of CAR between the cell types (Fig. 3).
Neg (not) Negative_regulation (limited) of in CAR Localization (localization) of Fig in cardiomyocytes associated with targeted disruption
3) Confidence 0.18 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.98 Pain Relevance 0.04
B-mediated transcriptional events completely prevented IL-6-mediated induction of Nox2 expression and superoxide production (Fig. 5b, c) and prevented the loss of GABAergic phenotype of PV-interneurons (Fig. 5d, e), as demonstrated by loss of PV and GAD67 immunoreactivity.
Negative_regulation (loss) of Localization (phenotype) of Fig in interneurons associated with gabaergic
4) Confidence 0.15 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.07 Pain Relevance 0.12
(Fig. 3A and 3B) and IL-6 (Fig. 3C and 3D) secretion is significantly reduced (p < 0.01).
Negative_regulation (reduced) of Localization (secretion) of Fig
5) Confidence 0.15 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2569027 Disease Relevance 0.18 Pain Relevance 0.14
We observed a reduced expression of this syntrophin in mdx5cv muscle (Fig. 7 B), similar to what was reported by Williams and Bloch (1999b).
Negative_regulation (reduced) of Localization (muscle) of Fig in muscle
6) Confidence 0.13 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2483333 Disease Relevance 0.06 Pain Relevance 0.12
Nuclear translocation (Fig. 5D) of Smad was decreased with myostatin inhibition and increased with myostatin overexpression.
Negative_regulation (decreased) of Localization (translocation) of Fig
7) Confidence 0.12 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2856679 Disease Relevance 0.05 Pain Relevance 0
(Fig. 6, panels A and B), but significantly reduced both IL-10 and IL-4 release (Fig. 6, panels C and D).
Negative_regulation (reduced) of Localization (release) of Fig
8) Confidence 0.11 Published 2008 Journal BMC Immunol Section Body Doc Link PMC2584092 Disease Relevance 0.16 Pain Relevance 0.07
The data presented in Fig. 1 and Table 1 show that exposure of muscle to oxypurinol induced a significant depression in maximum tetanic force generation by EDL and soleus muscles and a reduction in contraction-induced extracellular superoxide anion.
Negative_regulation (reduction) of Localization (presented) of Fig in muscles associated with depression
9) Confidence 0.11 Published 2010 Journal American Journal of Physiology - Regulatory, Integrative and Comparative Physiology Section Body Doc Link PMC2806206 Disease Relevance 0.25 Pain Relevance 0.05
(Fig. 3A and 3B) and IL-6 (Fig. 3C and 3D) secretion is significantly reduced (p < 0.01).
Negative_regulation (reduced) of Localization (secretion) of Fig
10) Confidence 0.11 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2569027 Disease Relevance 0.18 Pain Relevance 0.14
In the presence of ATP, the reduction in fluorescence upon KCl depolarization was markedly less, suggesting the attenuation of neurotransmitter release (Fig. 8, C, D, and G).
Negative_regulation (attenuation) of Localization (release) of Fig associated with neurotransmitter
11) Confidence 0.10 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2518726 Disease Relevance 0 Pain Relevance 0.17
Similarly, cytochrome c release (Fig. 8B) was also reduced in diabetic RAGE RAGE-KO, Tg DN PPET RAGE, and Tg DN MSR RAGE hearts versus diabetic wild-type hearts after I/R (P < 0.05).
Negative_regulation (reduced) of Localization (release) of Fig in hearts associated with targeted disruption and diabetes mellitus
12) Confidence 0.08 Published 2008 Journal Diabetes Section Body Doc Link PMC2453611 Disease Relevance 2.08 Pain Relevance 0
Secondly, THL could inhibit the secretion of pro-angiogenic factor by cancer cells (Fig 7).
Negative_regulation (inhibit) of Localization (secretion) of Fig associated with cancer
13) Confidence 0.06 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2880989 Disease Relevance 1.02 Pain Relevance 0.07
Zymography assays indicated that THL dose-dependently inhibited the secretion of MMP-2 (Fig 4C) and uPA (Fig 4D) in HMEC-1 cells.
Negative_regulation (inhibited) of Localization (secretion) of Fig associated with metalloproteinase
14) Confidence 0.06 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2880989 Disease Relevance 0.13 Pain Relevance 0.23
Zymography assays indicated that THL dose-dependently inhibited the secretion of MMP-2 (Fig 4C) and uPA (Fig 4D) in HMEC-1 cells.
Negative_regulation (inhibited) of Localization (secretion) of Fig associated with metalloproteinase
15) Confidence 0.06 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2880989 Disease Relevance 0.13 Pain Relevance 0.24
Moreover, APV also inhibited the strong depression induced by co-application of low NMDA and dopamine (Fig. 5D, E, F; F[3,70]?
Negative_regulation (depression) of Localization (application) of Fig associated with dopamine and depression
16) Confidence 0.04 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762427 Disease Relevance 0.32 Pain Relevance 1.00
-induced elevation in COX-2 Luciferase (Fig. 5C) and mRNA expression (Fig. 5D) was significantly inhibited by co-treatment of cells with the FP receptor antagonist (AL8810), and chemical inhibitors of PLC (U73122), PKA (4C3MQ), EGFR kinase (AG1478) and ERK1/2 kinase (PD98059), but not the EP2 receptor antagonist (AH6809), EP4 receptor antagonist (ONOAE2227) or PKC inhibitor (GF109203x; Fig. 5C and D, P < 0.05).


Negative_regulation (inhibited) of Localization (expression) of Fig associated with antagonist
17) Confidence 0.03 Published 2008 Journal Molecular and Cellular Endocrinology Section Body Doc Link PMC2694994 Disease Relevance 0 Pain Relevance 0.37
-induced elevation in COX-2 Luciferase (Fig. 5C) and mRNA expression (Fig. 5D) was significantly inhibited by co-treatment of cells with the FP receptor antagonist (AL8810), and chemical inhibitors of PLC (U73122), PKA (4C3MQ), EGFR kinase (AG1478) and ERK1/2 kinase (PD98059), but not the EP2 receptor antagonist (AH6809), EP4 receptor antagonist (ONOAE2227) or PKC inhibitor (GF109203x; Fig. 5C and D, P < 0.05).


Negative_regulation (inhibited) of Localization (expression) of Fig associated with antagonist
18) Confidence 0.03 Published 2008 Journal Molecular and Cellular Endocrinology Section Body Doc Link PMC2694994 Disease Relevance 0 Pain Relevance 0.37

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