INT4822

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Context Info
Confidence 0.80
First Reported 1980
Last Reported 2010
Negated 3
Speculated 2
Reported most in Body
Documents 417
Total Number 420
Disease Relevance 99.57
Pain Relevance 96.45

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

cytosol (Ca2) extracellular space (Ca2) lyase activity (Ca2)
response to stress (Ca2) cytoplasm (Ca2)
Anatomy Link Frequency
internal 28
reticulum 20
neurons 14
astrocytes 8
smooth muscle 8
Ca2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Action potential 894 100.00 Very High Very High Very High
Glutamate 755 100.00 Very High Very High Very High
Kinase C 670 100.00 Very High Very High Very High
gABA 426 100.00 Very High Very High Very High
Calcitonin gene-related peptide 414 100.00 Very High Very High Very High
Neurotransmitter 411 100.00 Very High Very High Very High
addiction 345 100.00 Very High Very High Very High
Opioid 277 100.00 Very High Very High Very High
noradrenaline 125 100.00 Very High Very High Very High
Endogenous opioid 43 100.00 Very High Very High Very High
Disease Link Frequency Relevance Heat
Hypertrophy 2169 99.92 Very High Very High Very High
Acidosis 1297 99.92 Very High Very High Very High
Stress 374 99.92 Very High Very High Very High
Nash(non-alcoholic Steatohepatitis) 48 99.92 Very High Very High Very High
Hypoxia 8511 99.86 Very High Very High Very High
Myocardial Infarction 750 99.76 Very High Very High Very High
Bordatella Infection 213 99.76 Very High Very High Very High
Cv Unclassified Under Development 1188 99.42 Very High Very High Very High
Rheumatoid Arthritis 8 99.40 Very High Very High Very High
Targeted Disruption 264 99.20 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The two types of spontaneous contractions were suggested to be triggered by different CA2+ release processes supposedly originating from different SR compartments.
Localization (release) of CA2
1) Confidence 0.80 Published 1986 Journal Eur. J. Pharmacol. Section Abstract Doc Link 3816944 Disease Relevance 0 Pain Relevance 0.30
In this process, Ca2+ influx through L-type Ca2+ channels (LCCs) on the cell surface membrane (including T-tubules) activates ryanodine receptor (RyR) Ca2+ release from the sarcoplasmic reticulum (SR) to generate cell-wide Ca2+ transients [7–9].
Localization (release) of Ca2 in tubules
2) Confidence 0.78 Published 2007 Journal PLoS Biology Section Body Doc Link PMC1764437 Disease Relevance 0.77 Pain Relevance 0
[The role of G protein in Leu-enkephalin induced Ca2+ release from intracellular pool in myocytes].
Localization (release) of Ca2 in myocytes associated with narcan and enkephalin
3) Confidence 0.78 Published 1995 Journal Sheng Li Xue Bao Section Title Doc Link 7652593 Disease Relevance 0 Pain Relevance 0.62
We can hypothesise that microglial activation promotes P2Y14 protein expression or coupling of the receptor to Ca2+ release.
Localization (release) of Ca2
4) Confidence 0.73 Published 2006 Journal Purinergic Signal Section Body Doc Link PMC2096653 Disease Relevance 0 Pain Relevance 0.12
activation and Ca2+ release through IP3 receptor/channels [43].
Localization (release) of Ca2
5) Confidence 0.73 Published 2006 Journal Purinergic Signal Section Body Doc Link PMC2096653 Disease Relevance 0 Pain Relevance 0.03
A model that has been advanced to explain hypoxic pulmonary vasoconstriction suggests that hypoxia-induced increase NADH could stimulate cyclic-ADP-ribose (cADPR) production (Dipp and Evans 2001; Evans and Dipp 2002). cADPR promotes Ca2+ release from the endoplasmic reticulum via ryanodine receptors (Galione 1993; Tanaka and Tashjian 1995; Thorn et al. 1994).
Localization (release) of Ca2 in reticulum associated with hypoxia and increased venous pressure under development
6) Confidence 0.73 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.79 Pain Relevance 0
This suggests that the Ca2+ uptake described here occurs via reversal of the principal pathway of mitochondrial Ca2+ release.
Localization (release) of Ca2
7) Confidence 0.71 Published 1985 Journal Arch. Biochem. Biophys. Section Abstract Doc Link 2415064 Disease Relevance 0 Pain Relevance 0.08
Approximately one-half of the sustained increase in fluorescence during 10 min of ischemia was caused by activation of Ca2+ release from mitochondria via the mitochondrial 2Na+-Ca2+ exchanger.
Localization (release) of Ca2 associated with ischemia
8) Confidence 0.70 Published 1999 Journal J. Neurosci. Section Abstract Doc Link 10212290 Disease Relevance 0.49 Pain Relevance 0.56
Pretreatment of thapsigargin in Ca2+-free solution fully inhibited the desipramine action, thus suggesting the involvement of Ca2+ release from intracellular Ca2+ stores at glutamatergic presynaptic nerve terminals.
Localization (release) of Ca2 in nerve associated with desipramine
9) Confidence 0.70 Published 2005 Journal Neurosci. Lett. Section Abstract Doc Link 15644283 Disease Relevance 0 Pain Relevance 0.79
The preceding studies with cyanide also indicate that inhibition of electron transport can promote Ca2+ release via another pathway (i.e., independent of mitochondrial depolarization).
Localization (release) of Ca2
10) Confidence 0.68 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.57 Pain Relevance 0
Although we have not investigated possible links between anoxia and ER function in any detail, it is notable that the anoxia-induced ER Ca2+ release persists in the presence of FCCP.
Localization (release) of Ca2 associated with hypoxia
11) Confidence 0.68 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.58 Pain Relevance 0
Anoxia increased [Ca2+]i by evoking Ca2+ release from two distinct internal stores one sensitive to carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP) and one sensitive to caffeine, cyclopiazonic acid (CPA), and ryanodine [assumed to be the endoplasmic reticulum (ER)].
Localization (release) of Ca2 in reticulum associated with hypoxia
12) Confidence 0.68 Published 2008 Journal Journal of Neurophysiology Section Abstract Doc Link PMC2493471 Disease Relevance 0.73 Pain Relevance 0.13
Evidence that anoxia enhances net Ca2+ release (or leak) from the ER comes primarily from our observation that the caffeine-releasable pool of Ca2+ progressively declines during anoxia (Fig. 9, A and B).
Localization (release) of Ca2 associated with hypoxia
13) Confidence 0.68 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.71 Pain Relevance 0
While this might indicate that anoxia inhibits mitochondrial Ca2+ release, there are other possible explanations (see following text).


Localization (release) of Ca2 associated with hypoxia
14) Confidence 0.68 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.70 Pain Relevance 0
Moreover, the observation that ryanodine prevented anoxia-induced release of Ca2+ from the ER suggests that Ca2+ efflux via ryanodine receptors plays an important role in mediating this slow ER Ca2+ release.
Localization (release) of Ca2 associated with hypoxia
15) Confidence 0.68 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.63 Pain Relevance 0
These observations suggest that inhibition of electron transport might be the key factor in promoting ER Ca2+ store release in response to anoxia and cyanide.
Localization (release) of Ca2 associated with hypoxia
16) Confidence 0.68 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.78 Pain Relevance 0
Moreover, the observation that ryanodine prevented anoxia-induced release of Ca2+ from the ER suggests that Ca2+ efflux via ryanodine receptors plays an important role in mediating this slow ER Ca2+ release.
Localization (release) of Ca2 associated with hypoxia
17) Confidence 0.68 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.62 Pain Relevance 0
To semi-quantify the amount of Ca2+ taken up by mitochondria, we used uncouplers to induce rapid mitochondrial Ca2+ release.
Localization (release) of Ca2
18) Confidence 0.68 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.31 Pain Relevance 0
While this could be due to a direct inhibition of mitochondrial Ca2+ release, it is also possible that it is simply an indirect consequence of reduced cytosolic Ca2+ clearance via PMCA and SERCA.
Localization (release) of Ca2
19) Confidence 0.68 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.38 Pain Relevance 0
Despite partially depolarizing mitochondria, anoxia had relatively little effect on mitochondrial Ca2+ uptake when neurons were depolarized but substantially delayed mitochondrial Ca2+ release and subsequent Ca2+ clearance from the cytosol on repolarization.
Localization (release) of Ca2 in neurons associated with hypoxia
20) Confidence 0.68 Published 2008 Journal Journal of Neurophysiology Section Abstract Doc Link PMC2493471 Disease Relevance 0.79 Pain Relevance 0.10

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