INT14546

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Context Info
Confidence 0.67
First Reported 1989
Last Reported 2010
Negated 1
Speculated 5
Reported most in Body
Documents 93
Total Number 98
Disease Relevance 31.09
Pain Relevance 18.72

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
reticulum 18
internal 6
tubules 4
mouth 4
heart 4
Ca2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Kinase C 221 100.00 Very High Very High Very High
Glutamate 96 100.00 Very High Very High Very High
Neurotransmitter 77 100.00 Very High Very High Very High
Enkephalin 11 100.00 Very High Very High Very High
b2 receptor 6 100.00 Very High Very High Very High
agonist 408 99.98 Very High Very High Very High
narcan 17 99.90 Very High Very High Very High
Clonidine 9 99.78 Very High Very High Very High
ischemia 326 99.70 Very High Very High Very High
Action potential 203 99.70 Very High Very High Very High
Disease Link Frequency Relevance Heat
Hypertrophy 567 100.00 Very High Very High Very High
Hypoxia 2837 99.98 Very High Very High Very High
Acidosis 198 99.92 Very High Very High Very High
Nash(non-alcoholic Steatohepatitis) 24 99.92 Very High Very High Very High
Myocardial Infarction 197 99.76 Very High Very High Very High
Bordatella Infection 94 99.76 Very High Very High Very High
Cv Unclassified Under Development 351 99.70 Very High Very High Very High
Stress 154 99.34 Very High Very High Very High
Low Back Pain 16 98.82 Very High Very High Very High
Disease 65 97.32 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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].
Positive_regulation (activates) of Localization (release) of Ca2 in tubules
1) Confidence 0.67 Published 2007 Journal PLoS Biology Section Body Doc Link PMC1764437 Disease Relevance 0.78 Pain Relevance 0
We can hypothesise that microglial activation promotes P2Y14 protein expression or coupling of the receptor to Ca2+ release.
Positive_regulation (promotes) of Localization (release) of Ca2
2) Confidence 0.63 Published 2006 Journal Purinergic Signal Section Body Doc Link PMC2096653 Disease Relevance 0 Pain Relevance 0.12
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.
Positive_regulation (promoting) of Localization (release) of Ca2 associated with hypoxia
3) Confidence 0.59 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.78 Pain Relevance 0
To semi-quantify the amount of Ca2+ taken up by mitochondria, we used uncouplers to induce rapid mitochondrial Ca2+ release.
Positive_regulation (induce) of Localization (release) of Ca2
4) Confidence 0.59 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.31 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.
Positive_regulation (mediating) of Localization (release) of Ca2 associated with hypoxia
5) Confidence 0.59 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.63 Pain Relevance 0
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).
Positive_regulation (promote) of Localization (release) of Ca2
6) Confidence 0.59 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.57 Pain Relevance 0
According to these first studies, activation of the former caused inward currents and depolarisation of membrane potential and activation of the latter induced a K+ outward current and Ca2+ release [36–38].
Positive_regulation (induced) of Localization (release) of Ca2
7) Confidence 0.55 Published 2006 Journal Purinergic Signal Section Body Doc Link PMC2096653 Disease Relevance 0 Pain Relevance 0.04
Figure 4Pertussis toxin completely inhibits Ca2+ release induced by adenine nucleotides but not by uridine 5?
Positive_regulation (induced) of Localization (release) of Ca2
8) Confidence 0.55 Published 2006 Journal Purinergic Signal Section Body Doc Link PMC2096653 Disease Relevance 0.08 Pain Relevance 0.04
When we utilised the protonophore FCCP, known to cause mitochondrial depolarisation, we could clearly see a decrease of oscillatory Ca2+ release induced by low doses of UTP.
Positive_regulation (induced) of Localization (release) of Ca2
9) Confidence 0.55 Published 2006 Journal Purinergic Signal Section Body Doc Link PMC2096653 Disease Relevance 0 Pain Relevance 0
[The role of G protein in Leu-enkephalin induced Ca2+ release from intracellular pool in myocytes].
Positive_regulation (role) of Localization (release) of Ca2 in myocytes associated with narcan and enkephalin
10) Confidence 0.49 Published 1995 Journal Sheng Li Xue Bao Section Title Doc Link 7652593 Disease Relevance 0 Pain Relevance 0.62
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.
Positive_regulation (activation) of Localization (release) of Ca2 associated with ischemia
11) Confidence 0.47 Published 1999 Journal J. Neurosci. Section Abstract Doc Link 10212290 Disease Relevance 0.49 Pain Relevance 0.56
activation and Ca2+ release through IP3 receptor/channels [43].
Positive_regulation (activation) of Localization (release) of Ca2
12) Confidence 0.46 Published 2006 Journal Purinergic Signal Section Body Doc Link PMC2096653 Disease Relevance 0 Pain Relevance 0.03
Hypoxia-evoked ER Ca2+ release in astrocytes has also recently been attributed to cADPR-mediated activation of ryanodine receptors (Aley et al. 2006).
Positive_regulation (activation) of Localization (release) of Ca2 in astrocytes associated with hypoxia
13) Confidence 0.43 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.78 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)].
Positive_regulation (increased) of Localization (release) of Ca2 in reticulum associated with hypoxia
14) Confidence 0.43 Published 2008 Journal Journal of Neurophysiology Section Abstract Doc Link PMC2493471 Disease Relevance 0.74 Pain Relevance 0.13
The observation that part of the [Ca2+]i response to anoxia was abolished by application of FCCP led us to further investigate the role of mitochondria in mediating Ca2+ release.
Spec (investigate) Positive_regulation (mediating) of Localization (release) of Ca2 associated with hypoxia
15) Confidence 0.43 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.60 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.
Positive_regulation (induced) of Localization (release) of Ca2 associated with hypoxia
16) Confidence 0.43 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.58 Pain Relevance 0
The preceding data suggested that part of the response to anoxia could be mediated by Ca2+ release from caffeine-sensitive internal stores.
Positive_regulation (mediated) of Localization (release) of Ca2 in internal associated with hypoxia
17) Confidence 0.43 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.76 Pain Relevance 0
These data suggest that both anoxia and cyanide might induce some Ca2+ release through mitochondrial depolarization.
Spec (might) Positive_regulation (induce) of Localization (release) of Ca2 associated with hypoxia
18) Confidence 0.43 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.68 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.
Positive_regulation (induced) of Localization (release) of Ca2 associated with hypoxia
19) Confidence 0.43 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.63 Pain Relevance 0
This secondary phase, or shoulder, in [Ca2+]i has been attributed to the release of Ca2+ from mitochondria that had previously been accumulated during exposure to high K+ when [Ca2+]i is very high (Werth and Thayer 1994).
Positive_regulation (accumulated) of Localization (release) of Ca2 in shoulder
20) Confidence 0.43 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.32 Pain Relevance 0.03

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