INT33094

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Context Info
Confidence 0.38
First Reported 1985
Last Reported 2010
Negated 7
Speculated 1
Reported most in Body
Documents 28
Total Number 29
Disease Relevance 8.65
Pain Relevance 9.96

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
neurons 6
thymocytes 2
internal 2
lactotrophs 2
somas 2
Ca2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Calcitonin gene-related peptide 66 99.92 Very High Very High Very High
tetrodotoxin 60 99.48 Very High Very High Very High
Morphine 130 99.36 Very High Very High Very High
pregabalin 800 99.34 Very High Very High Very High
qutenza 249 99.04 Very High Very High Very High
Action potential 64 98.88 Very High Very High Very High
dorsal root ganglion 345 97.88 Very High Very High Very High
narcan 70 96.76 Very High Very High Very High
adenocard 42 96.16 Very High Very High Very High
Norepinephrine uptake inhibitor 1 94.80 High High
Disease Link Frequency Relevance Heat
Hypoxia 1428 100.00 Very High Very High Very High
Ganglion Cysts 363 97.88 Very High Very High Very High
Myocardial Infarction 4 91.76 High High
Heart Rate Under Development 1 89.76 High High
Acidosis 168 87.68 High High
Apoptosis 25 86.68 High High
Nociception 63 81.76 Quite High
Cv Unclassified Under Development 148 76.04 Quite High
Lymphatic System Cancer 2 75.52 Quite High
B-cell Acute Lymphoblastic Leukemia 1 75.16 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We cannot, however, exclude the possibility that other mechanisms also contribute to ER Ca2+ release.
Spec (possibility) Regulation (contribute) of Localization (release) of Ca2
1) Confidence 0.38 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.75 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.
Neg (little) Regulation (effect) of Localization (release) of Ca2 in neurons associated with hypoxia
2) Confidence 0.38 Published 2008 Journal Journal of Neurophysiology Section Abstract Doc Link PMC2493471 Disease Relevance 0.82 Pain Relevance 0.11
Effects of anoxia on mitochondrial Ca2+ buffering
Regulation (Effects) of Localization (buffering) of Ca2 associated with hypoxia
3) Confidence 0.38 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.75 Pain Relevance 0.05
Interactions among the effects of anoxia on Ca2+ clearance, mitochondrial Ca2+ buffering, and ER Ca2+ uptake
Regulation (effects) of Localization (buffering) of Ca2 associated with hypoxia
4) Confidence 0.38 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.49 Pain Relevance 0
Because this could not be attributed to an increased mitochondrial Ca2+ load, it must reflect some effect of anoxia on mitochondrial Ca2+ release or cytosolic Ca2+ clearance/extrusion mechanisms.
Regulation (effect) of Localization (release) of Ca2 associated with hypoxia
5) Confidence 0.38 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.28 Pain Relevance 0
Because this could not be attributed to an increased mitochondrial Ca2+ load, it must reflect some effect of anoxia on mitochondrial Ca2+ release or cytosolic Ca2+ clearance/extrusion mechanisms.
Regulation (effect) of Localization (release) of Ca2 associated with hypoxia
6) Confidence 0.38 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.28 Pain Relevance 0
Determining which of these pathways are indeed responsible for the sustained Ca2+ release from internal stores seen acidic conditions clearly requires further investigation.


Regulation (responsible) of Localization (release) of Ca2 in internal
7) Confidence 0.37 Published 2009 Journal Pflugers Arch Section Body Doc Link PMC2765625 Disease Relevance 0.90 Pain Relevance 0.04
The Ca2+ plateau induced by UTP was abrogated by SKF96395, depicting the nature of the plateau phase, while the Ca2+ peak (due to Ca2+ release) was unaffected (n = 81).
Neg (unaffected) Regulation (unaffected) of Localization (release) of Ca2
8) Confidence 0.36 Published 2006 Journal Purinergic Signal Section Body Doc Link PMC2096653 Disease Relevance 0 Pain Relevance 0.07
The Ca2+ plateau induced by UTP was abrogated by SKF96395, depicting the nature of the plateau phase, while the Ca2+ peak (due to Ca2+ release) was unaffected (n = 81).
Neg (unaffected) Regulation (unaffected) of Localization (release) of Ca2
9) Confidence 0.36 Published 2006 Journal Purinergic Signal Section Body Doc Link PMC2096653 Disease Relevance 0 Pain Relevance 0.07
Effect of thiopental on intracellular Ca2+ concentration
Regulation (Effect) of Localization (concentration) of Ca2
10) Confidence 0.26 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2824862 Disease Relevance 1.20 Pain Relevance 0
These data suggest that the elevated concentration of sodium ions could effect Na+/Ca2+ exchange and provoke Ca2+ release from sarcoplasmic reticulum by changing the sodium gradient and resulting in Ca2+ entry via Na+/Ca2+ exchange.
Regulation (effect) of Localization (release) of Ca2 in reticulum
11) Confidence 0.24 Published 2001 Journal Fiziol Zh Section Abstract Doc Link 11296555 Disease Relevance 0.09 Pain Relevance 0.11
We briefly investigated whether mitochondrial Ca2+ buffering could influence ER store loading by looking at the effects of FCCP on store loading and caffeine-evoked Ca2+ release.
Regulation (effects) of Localization (release) of Ca2
12) Confidence 0.23 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.44 Pain Relevance 0
The effects of anoxia on DRG neurons were not limited to Ca2+ store release; however, it also had multiple other effects on [Ca2+]i regulation (see following text).
Regulation (effects) of Localization (release) of Ca2 in neurons associated with hypoxia
13) Confidence 0.23 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.83 Pain Relevance 0.18
Effects of anoxia on ER Ca2+ release
Regulation (Effects) of Localization (release) of Ca2 associated with hypoxia
14) Confidence 0.23 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.73 Pain Relevance 0
The effect of ouabain was compared with the effects of high K+ and the Ca2+ ionophore A23187. [3H]Norepinephrine release elicited by depolarization with high extracellular K+ was dependent on extracellular Ca2+, was unaffected by tetrodotoxin, was potentiated by reducing extracellular Na+, and was potentiated by the norepinephrine uptake inhibitor desipramine.
Regulation (dependent) of Localization (release) of Ca2 associated with tetrodotoxin, desipramine and norepinephrine uptake inhibitor
15) Confidence 0.21 Published 1985 Journal J. Neurosci. Section Abstract Doc Link 2993543 Disease Relevance 0 Pain Relevance 0.19
The release of CGRP is dependent on extra-cellular Ca2+ and Ca2+-induced Ca2+ release from the intracellular Ca2+ store which is sensitive to ruthenium red.
Regulation (dependent) of Localization (release) of Ca2 associated with calcitonin gene-related peptide
16) Confidence 0.19 Published 1996 Journal Sheng Li Xue Bao Section Abstract Doc Link 8758688 Disease Relevance 0.12 Pain Relevance 0.74
Modulation of either Ca2+-induced Ca2+ release and / or Ca2+ homeostatic mechanisms might provide a mechanism by which pregabalin enhanced Ca2+ transients in neurones with intermediate and large sized cell somas.
Regulation (Modulation) of Localization (release) of Ca2 in somas associated with pregabalin
17) Confidence 0.19 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC514605 Disease Relevance 0.16 Pain Relevance 0.78
Alternatively, pregabalin could potentially have a direct or indirect influence on Ca2+-induced Ca2+ release from intracellular stores and alter Ca2+ homeostatic mechanisms.
Regulation (influence) of Localization (release) of Ca2 associated with pregabalin
18) Confidence 0.19 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC514605 Disease Relevance 0.14 Pain Relevance 1.09
These apparent anomalies seen with pregabalin do not appear to be due to drug effects on Ca2+-induced Ca2+ release or Ca2+ homeostatic mechanisms such as Na+/Ca2+ exchange.
Regulation (effects) of Localization (release) of Ca2 associated with pregabalin
19) Confidence 0.19 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC514605 Disease Relevance 0.17 Pain Relevance 0.89
In conclusion these results indicate that modulation of Ca2+-induced Ca2+ release and Ca2+ homeostatic mechanisms do not account for pregabalin-induced enhancement of K+-evoked Ca2+ flux in a population of DRG neurones.
Regulation (modulation) of Localization (release) of Ca2 associated with dorsal root ganglion and pregabalin
20) Confidence 0.19 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC514605 Disease Relevance 0.37 Pain Relevance 0.75

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