INT25170

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.67
First Reported 1984
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 78
Total Number 78
Disease Relevance 15.25
Pain Relevance 11.24

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

cytosol (Car2) extracellular space (Car2) lyase activity (Car2)
cytoplasm (Car2)
Anatomy Link Frequency
myotubes 14
internal 9
reticulum 8
skeletal muscle 6
smooth muscle 4
Car2 (Mus musculus)
Pain Link Frequency Relevance Heat
agonist 471 100.00 Very High Very High Very High
addiction 168 100.00 Very High Very High Very High
cINOD 296 99.10 Very High Very High Very High
tetrodotoxin 28 99.00 Very High Very High Very High
depression 104 98.64 Very High Very High Very High
antagonist 358 98.48 Very High Very High Very High
Neurotransmitter 175 98.16 Very High Very High Very High
Calcium channel 47 96.32 Very High Very High Very High
Morphine 247 96.04 Very High Very High Very High
adenocard 21 95.28 Very High Very High Very High
Disease Link Frequency Relevance Heat
Stress 90 100.00 Very High Very High Very High
Systemic Lupus Erythematosus 2 99.68 Very High Very High Very High
Disease 448 99.10 Very High Very High Very High
Depression 107 98.64 Very High Very High Very High
Nociception 61 97.96 Very High Very High Very High
Contracture 37 97.84 Very High Very High Very High
Drug Induced Neurotoxicity 84 97.04 Very High Very High Very High
Death 336 96.84 Very High Very High Very High
Autoimmune Disease 20 96.64 Very High Very High Very High
Adverse Drug Reaction 7 92.64 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We conclude that cerebellar Bergmann glial cells are endowed with alpha1-adrenoreceptors and H1 histamine receptors which induce the generation of intracellular [Ca2+]i signals via activation of Ca2+ release from inositol-1,4,5-trisphosphate-sensitive intracellular stores.
Positive_regulation (activation) of Localization (release) of Ca2 in Bergmann glial cells
1) Confidence 0.67 Published 1996 Journal Eur. J. Neurosci. Section Abstract Doc Link 8752590 Disease Relevance 0 Pain Relevance 0.58
Stimulating a single glial cell leads to the production of InsP3, triggering the release of Ca2+ from internal stores in the stimulated cell as well as in adjacent cells.
Positive_regulation (triggering) of in glial cell Localization (release) of Ca2 in internal
2) Confidence 0.46 Published 2005 Journal Purinergic Signal Section Body Doc Link PMC2096541 Disease Relevance 0 Pain Relevance 0
All of these drugs inhibited the medium ADP, suggesting the Ca2+ release is required for the medium ADP, but not the slow ADP.
Positive_regulation (required) of Localization (release) of Ca2
3) Confidence 0.41 Published 2010 Journal PLoS Biology Section Body Doc Link PMC2982802 Disease Relevance 0 Pain Relevance 0.14
This process of Ca2+ uptake by the sarcoplasmic reticulum via Ca2+-ATPase reduces intramuscular Ca2+ concentrations and results in muscle relaxation.6,7
Positive_regulation (uptake) of Localization (reticulum) of Ca2 in reticulum
4) Confidence 0.41 Published 2006 Journal Yonsei Medical Journal Section Body Doc Link PMC2687630 Disease Relevance 0.36 Pain Relevance 0
Therefore, we postulate that the selenite-induced contracture was induced by the initial binding of selenite to the sulfhydryl groups of the muscle membrane, which then triggered the release of Ca2+ from internal membranes such as the sarcoplasmic reticulum.
Positive_regulation (triggered) of Localization (release) of Ca2 in internal associated with contracture
5) Confidence 0.41 Published 1989 Journal Eur. J. Pharmacol. Section Abstract Doc Link 2506065 Disease Relevance 0.83 Pain Relevance 0.03
However, depolarization of the islet with KCl in low Ca(2+)-containing solutions induced intracellular Ca2+ release, which was resistant to tetrodotoxin.
Positive_regulation (induced) of Localization (release) of Ca2 associated with tetrodotoxin
6) Confidence 0.40 Published 1993 Journal J. Biol. Chem. Section Abstract Doc Link 8387528 Disease Relevance 0 Pain Relevance 0.24
Moreover, because muscle contractility in primary IOOA is presumed to be larger than that of normal controls, intramuscular Ca2+ concentrations in primary IOOA are expected to be higher than normal, which suggests Ca2+ release by the sarcoplasmic reticulum is enhenced.
Positive_regulation (enhenced) of Localization (release) of Ca2 in muscle
7) Confidence 0.36 Published 2006 Journal Yonsei Medical Journal Section Body Doc Link PMC2687630 Disease Relevance 0.30 Pain Relevance 0.03
In most cases, synaptic plasticity is induced by an increase in intracellular Ca2+ concentration ([Ca2+]i) and regulated by complex downstream molecular networks consisting of numerous molecules such as protein kinases and phosphatases (Malenka and Nicoll, 1999; Lisman et al, 2002; Sheng and Kim, 2002).
Positive_regulation (increase) of Localization (concentration) of Ca2
8) Confidence 0.34 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0.11 Pain Relevance 0.16
This view is supported by i)the chemical structure of NSAIDs resembling mitochondrial uncouplers, ii)the release of Ca2+ induced by salicylate in Ca2+-overloaded cells and iii)direct TMRM fluorescence measurements showing NSAID-induced mitochondrial depolarization.
Positive_regulation (induced) of Localization (release) of Ca2 associated with cinod
9) Confidence 0.30 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2447871 Disease Relevance 0.43 Pain Relevance 0.46
Under these conditions, veratridine also stimulated the Ca2+ independent release of choline, and this increase exceeded that obtained for the Ca2+-independent release of ACh.
Positive_regulation (stimulated) of Localization (release) of Ca2
10) Confidence 0.27 Published 1984 Journal Brain Res. Section Abstract Doc Link 6697191 Disease Relevance 0 Pain Relevance 0.09
Overall, these data from inside-out patches and RT-PCR identified the presence of Ca2+-activated Cl?
Positive_regulation (activated) of Localization (presence) of Ca2
11) Confidence 0.26 Published 2010 Journal The Journal of General Physiology Section Body Doc Link PMC2806418 Disease Relevance 0 Pain Relevance 0
To confirm the presence of Ca2+-activated Cl?
Positive_regulation (activated) of Localization (presence) of Ca2
12) Confidence 0.26 Published 2010 Journal The Journal of General Physiology Section Body Doc Link PMC2806418 Disease Relevance 0 Pain Relevance 0.03
ACh (0.1-3 mM, 20 microliters) elicited bi-phasic elevation of [Ca2+]i (fast and slow Ca2+ mobilization measured as Ca(2+)-aequorin luminescence) in muscle cells.
Positive_regulation (elevation) of Localization (mobilization) of Ca2 in muscle cells
13) Confidence 0.26 Published 1997 Journal Nippon Yakurigaku Zasshi Section Abstract Doc Link 9503417 Disease Relevance 0 Pain Relevance 0.11
We have found that non-contractile slow Ca2+ mobilization (RAMIC; Receptor-Activity Modulating Intracellular Ca2+) is generated by motor nerve stimulation with anti-cholinesterase at the skeletal muscle, and desensitizes muscle nicotinic receptor (nAChR).
Positive_regulation (generated) of Localization (mobilization) of Ca2 in skeletal muscle
14) Confidence 0.26 Published 1997 Journal Nippon Yakurigaku Zasshi Section Abstract Doc Link 9503417 Disease Relevance 0 Pain Relevance 0
For example, Ca2+ entry and release from internal stores could activate nonselective cation currents, such as ICAN, which mediate the medium ADP.
Positive_regulation (activate) of Localization (release) of Ca2 in internal
15) Confidence 0.26 Published 2010 Journal PLoS Biology Section Body Doc Link PMC2982802 Disease Relevance 0 Pain Relevance 0.12
For example, in familial AD, loss of function presenilin 1 mutants show exaggerated Ca2+ release from intracellular stores due to either defective Ca2+ leak from the ER or increased activity of Ca2+ release channels at ER [48–50, but see also 51 for alternative results].
Positive_regulation (increased) of Localization (release) of Ca2 associated with disease
16) Confidence 0.25 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2447871 Disease Relevance 0.29 Pain Relevance 0.07
For example, in familial AD, loss of function presenilin 1 mutants show exaggerated Ca2+ release from intracellular stores due to either defective Ca2+ leak from the ER or increased activity of Ca2+ release channels at ER [48–50, but see also 51 for alternative results].
Positive_regulation (exaggerated) of Localization (release) of Ca2 associated with disease
17) Confidence 0.25 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2447871 Disease Relevance 0.29 Pain Relevance 0.07
Besides the severely impaired SOCE, we also observed reduced Ca2+ release from intracellular stores upon agonist-induced platelet activation, which likely reflects a lower filling state of the SR, as shown by passively emptying the stores with the SERCA inhibitor TG (Fig. 1 E).
Positive_regulation (induced) of Localization (release) of Ca2 in platelet associated with agonist
18) Confidence 0.25 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2442636 Disease Relevance 0 Pain Relevance 0.08
One candidate molecule is STIM2, which has been shown to activate Ca2+ release–activated channels (21).
Positive_regulation (activate) of Localization (release) of Ca2
19) Confidence 0.25 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2442636 Disease Relevance 0.11 Pain Relevance 0.08
Therefore, one possible explanation for the increased response to ACh of OA-challenged BSMs may be attributable to an enhanced Ca2+ mobilization in BSM cells.
Positive_regulation (enhanced) of Localization (mobilization) of Ca2
20) Confidence 0.24 Published 2005 Journal Respir Res Section Body Doc Link PMC545934 Disease Relevance 0 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox