INT17561

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Context Info
Confidence 0.79
First Reported 1984
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 303
Total Number 303
Disease Relevance 60.95
Pain Relevance 44.52

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
reticulum 21
internal 15
myotubes 15
muscle 7
astrocytes 6
Car2 (Mus musculus)
Pain Link Frequency Relevance Heat
antagonist 883 100.00 Very High Very High Very High
Glutamate 825 100.00 Very High Very High Very High
Neurotransmitter 514 100.00 Very High Very High Very High
adenocard 212 100.00 Very High Very High Very High
Catecholamine 54 100.00 Very High Very High Very High
Enkephalin 6 100.00 Very High Very High Very High
addiction 582 99.92 Very High Very High Very High
mu opioid receptor 4 99.90 Very High Very High Very High
Morphine 357 99.84 Very High Very High Very High
Kinase C 101 99.84 Very High Very High Very High
Disease Link Frequency Relevance Heat
Nociception 126 100.00 Very High Very High Very High
Pheochromocytoma 48 99.84 Very High Very High Very High
Stress 584 99.70 Very High Very High Very High
Systemic Lupus Erythematosus 3 99.68 Very High Very High Very High
Apoptosis 944 99.40 Very High Very High Very High
Contracture 100 99.34 Very High Very High Very High
Cataract 9 99.32 Very High Very High Very High
Disease 2377 99.00 Very High Very High Very High
Obesity 588 99.00 Very High Very High Very High
Malignant Hyperthermia 401 98.82 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
CAIV activity was recently demonstrated in the ciliary processes [73] and so our data may support a more substantial role for CAIV compared to CAII in aqueous humor secretion.
Localization (secretion) of CAII in ciliary
1) Confidence 0.79 Published 2001 Journal BMC Genet Section Body Doc Link PMC48141 Disease Relevance 0.87 Pain Relevance 0
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.
Localization (release) of Ca2 in Bergmann glial cells
2) Confidence 0.78 Published 1996 Journal Eur. J. Neurosci. Section Abstract Doc Link 8752590 Disease Relevance 0 Pain Relevance 0.57
Therefore, the possible involvement of Ca2+ release from intracellular Ca2+ stores to prolong the [Ca2+]i transients under bicuculline administration cannot be excluded completely.
Localization (release) of Ca2
3) Confidence 0.78 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2966408 Disease Relevance 0 Pain Relevance 0.12
These remaining responses might include the Ca2+ release from intracellular Ca2+ stores via activation of the G-protein coupled receptors such as metabotropic glutamate receptors.
Localization (release) of Ca2 associated with glutamate receptor
4) Confidence 0.68 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2966408 Disease Relevance 0 Pain Relevance 0.29
Therefore, the possible involvement of Ca2+ release from intracellular Ca2+ stores to prolong the [Ca2+]i transients under bicuculline administration cannot be excluded completely.
Localization (release) of Ca2
5) Confidence 0.68 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2966408 Disease Relevance 0 Pain Relevance 0.12
These remaining responses might include the Ca2+ release from intracellular Ca2+ stores via activation of the G-protein coupled receptors such as metabotropic glutamate receptors.
Localization (release) of Ca2 associated with glutamate receptor
6) Confidence 0.68 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2966408 Disease Relevance 0 Pain Relevance 0.29
This process of Ca2+ uptake by the sarcoplasmic reticulum via Ca2+-ATPase reduces intramuscular Ca2+ concentrations and results in muscle relaxation.6,7
Localization (reticulum) of Ca2 in reticulum
7) Confidence 0.62 Published 2006 Journal Yonsei Medical Journal Section Body Doc Link PMC2687630 Disease Relevance 0.35 Pain Relevance 0
Tail-flick latencies at 35 and 50 V in diabetic mice were increased by pretreatment with ryanodine, which blocks Ca2+ release from Ca2+/caffeine-sensitive microsomal pools.
Localization (release) of Ca2 in Tail associated with diabetes mellitus and tail-flick
8) Confidence 0.62 Published 1999 Journal Brain Res. Section Abstract Doc Link 10375704 Disease Relevance 1.08 Pain Relevance 0.69
Tail-flick latencies at 35 and 50 V in diabetic mice were increased by pretreatment with ryanodine, which blocks Ca2+ release from Ca2+/caffeine-sensitive microsomal pools.
Localization (release) of Ca2 in Tail associated with diabetes mellitus and tail-flick
9) Confidence 0.62 Published 1999 Journal Brain Res. Section Abstract Doc Link 10375704 Disease Relevance 1.08 Pain Relevance 0.69
Pools of intracellular Ca2+ were released to the extracellular compartment, where they reacted with the dye by sequential treatment of the cells with m-fluorocarbonylcyanidediphenylhydrazone (FCCP) and the Ca2+-ionophore A23187.
Localization (released) of Ca2
10) Confidence 0.62 Published 1987 Journal Eur J Cancer Clin Oncol Section Abstract Doc Link 2439346 Disease Relevance 0.50 Pain Relevance 0
All of these findings suggest that the selenite contracture was not dependent on external Ca2+ but was induced by the release of Ca2+ from internal membranes such as the sarcoplasmic reticulum.
Localization (release) of Ca2 in internal associated with contracture
11) Confidence 0.61 Published 1989 Journal Eur. J. Pharmacol. Section Abstract Doc Link 2506065 Disease Relevance 0.98 Pain Relevance 0.09
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.
Localization (release) of Ca2 in internal associated with contracture
12) Confidence 0.61 Published 1989 Journal Eur. J. Pharmacol. Section Abstract Doc Link 2506065 Disease Relevance 0.82 Pain Relevance 0.03
Ca2+ is accumulated in intracellular stores by means of Ca2+ pumps and is released via inositol 1,4,5-trisphosphate (IP3) and ryanodine receptors.
Localization (released) of Ca2
13) Confidence 0.61 Published 2000 Journal Verh. K. Acad. Geneeskd. Belg. Section Abstract Doc Link 11196578 Disease Relevance 0.93 Pain Relevance 0
Ca2+ can come from the extracellular space or be released from intracellular stores.
Localization (released) of Ca2
14) Confidence 0.61 Published 2000 Journal Verh. K. Acad. Geneeskd. Belg. Section Abstract Doc Link 11196578 Disease Relevance 0.42 Pain Relevance 0
The results suggest that pacemaker [Ca2+]i oscillations in ICCs are produced by close interaction of intracellular Ca2+ release channels, especially inositol 1,4,5-trisphosphate receptor (InsP3R) and Ca2+ influx pathways, presumably corresponding to store-operated type channels.
Localization (release) of Ca2
15) Confidence 0.61 Published 2005 Journal J. Biol. Rhythms Section Abstract Doc Link 15654067 Disease Relevance 0 Pain Relevance 0.11
Using fura-2-loaded mouse islets, we demonstrate, in fact, that the major component of the glucose-activated [Ca2+]i rise represents voltage-dependent intracellular Ca2+ release.
Localization (release) of Ca2
16) Confidence 0.61 Published 1993 Journal J. Biol. Chem. Section Abstract Doc Link 8387528 Disease Relevance 0 Pain Relevance 0.20
In the absence of external Ca2+, glucose still caused intracellular Ca2+ release, an effect blockable by tetrodotoxin.
Localization (release) of Ca2 in external associated with tetrodotoxin
17) Confidence 0.61 Published 1993 Journal J. Biol. Chem. Section Abstract Doc Link 8387528 Disease Relevance 0 Pain Relevance 0.23
Furthermore, the Ca2+ release pool possesses a novel pharmacology in that it is caffeine-sensitive but ryanodine-insensitive.
Localization (release) of Ca2
18) Confidence 0.61 Published 1993 Journal J. Biol. Chem. Section Abstract Doc Link 8387528 Disease Relevance 0 Pain Relevance 0.20
We conclude that glucose release of intracellular Ca2+ is dependent upon depolarization alone, possibly through increasing inositol 1,4,5-trisphosphate production.
Localization (release) of Ca2
19) Confidence 0.61 Published 1993 Journal J. Biol. Chem. Section Abstract Doc Link 8387528 Disease Relevance 0 Pain Relevance 0.23
Using fura-2-loaded mouse islets, we demonstrate, in fact, that the major component of the glucose-activated [Ca2+]i rise represents voltage-dependent intracellular Ca2+ release.
Localization (release) of Ca2
20) Confidence 0.61 Published 1993 Journal J. Biol. Chem. Section Abstract Doc Link 8387528 Disease Relevance 0 Pain Relevance 0.20

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