INT74051

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Context Info
Confidence 0.38
First Reported 1997
Last Reported 2010
Negated 0
Speculated 2
Reported most in Body
Documents 27
Total Number 30
Disease Relevance 9.58
Pain Relevance 5.10

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
cardiomyocytes 4
platelet 4
myocyte 4
CPA 4
myotubes 4
Car2 (Mus musculus)
Pain Link Frequency Relevance Heat
tetrodotoxin 16 99.98 Very High Very High Very High
Nicotine 7 99.08 Very High Very High Very High
agonist 79 98.72 Very High Very High Very High
cINOD 149 98.46 Very High Very High Very High
antagonist 54 98.16 Very High Very High Very High
tail-flick 3 98.08 Very High Very High Very High
Spinal cord 9 98.04 Very High Very High Very High
Action potential 73 97.84 Very High Very High Very High
anesthesia 16 97.20 Very High Very High Very High
intrathecal 3 94.64 High High
Disease Link Frequency Relevance Heat
Stress 124 99.56 Very High Very High Very High
Obesity 169 99.50 Very High Very High Very High
Disease 409 99.00 Very High Very High Very High
Diabetes Mellitus 23 98.82 Very High Very High Very High
Aging 143 98.16 Very High Very High Very High
Death 184 97.68 Very High Very High Very High
Drug Induced Neurotoxicity 42 97.44 Very High Very High Very High
Renal Failure 2 97.36 Very High Very High Very High
Malignant Hyperthermia 47 97.04 Very High Very High Very High
Apoptosis 91 95.84 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Several factors may contribute to the impaired mechanical function including defected contractile proteins (e.g., actin, myosin heavy chain isoform), reduced intracellular Ca2+ release, depressed SR Ca2+ load and altered myofilament Ca2+ sensitivity.
Negative_regulation (reduced) of Localization (release) of Ca2
1) Confidence 0.38 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2696039 Disease Relevance 0.54 Pain Relevance 0.03
Cardiomyocytes from APP/PS1 mice exhibited decreased inotropic response and impaired intracellular Ca2+ homeostasis possibly due to mechanisms associated with reduced intracellular Ca2+ release, altered expression in Ca2+ regulatory proteins, reduced adrenergic function and oxidative damage.
Negative_regulation (reduced) of Localization (release) of Ca2 in Cardiomyocytes
2) Confidence 0.38 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2696039 Disease Relevance 1.13 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.
Negative_regulation (blocks) of Localization (release) of Ca2 in Tail associated with diabetes mellitus and tail-flick
3) Confidence 0.38 Published 1999 Journal Brain Res. Section Abstract Doc Link 10375704 Disease Relevance 1.08 Pain Relevance 0.69
Neither nicotine nor choline produced Ca2+ increase following inhibition of the release of Ca2+ from intracellular stores by dantrolene.
Negative_regulation (inhibition) of Localization (release) of Ca2 associated with nicotine
4) Confidence 0.36 Published 2000 Journal Eur. J. Neurosci. Section Abstract Doc Link 10947823 Disease Relevance 0 Pain Relevance 0.76
Thus, we postulated that, in primary IOOA, the Ca2+ storage within the sarcoplasmic reticulum is reduced due to Ca2+-ATPase inactivation, and that consequently Ca2+-release capacity is reduced.
Negative_regulation (reduced) of Localization (release) of Ca2 in reticulum
5) Confidence 0.31 Published 2006 Journal Yonsei Medical Journal Section Body Doc Link PMC2687630 Disease Relevance 0.31 Pain Relevance 0.03
Blocking Ca2+ release from internal stores with cyclopiazonic acid (CPA; 20 µM) also reduced the medium ADP (Figure S6), suggesting that this is another important mechanism for induction of the medium ADP.
Negative_regulation (reduced) of Localization (release) of Ca2 in CPA
6) Confidence 0.30 Published 2010 Journal PLoS Biology Section Body Doc Link PMC2982802 Disease Relevance 0 Pain Relevance 0.17
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).
Negative_regulation (reduced) of Localization (release) of Ca2 in platelet associated with agonist
7) Confidence 0.29 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2442636 Disease Relevance 0 Pain Relevance 0.08
In addition, our data revealed exaggerated decline in the steady-state myocyte peak shortening in response to increased stimulating frequency in APP/PS1 mice, suggesting a possibly reduced capacity in SR Ca2+ storage and release in this murine model of AD.
Spec (possibly) Negative_regulation (capacity) of Localization (release) of Ca2 in myocyte associated with disease
8) Confidence 0.28 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2696039 Disease Relevance 0.20 Pain Relevance 0
Relative quantification of Ca2+ and NO signals
Negative_regulation (Relative) of Localization (quantification) of Ca2
9) Confidence 0.27 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2659787 Disease Relevance 0.24 Pain Relevance 0.09
Neither Ca2+ channel blockers nor a Na+ channel blocker tetrodotoxin prevented the generation of the slow Ca2+ mobilization.
Negative_regulation (prevented) of Localization (mobilization) of Ca2 associated with tetrodotoxin
10) Confidence 0.24 Published 1997 Journal Nippon Yakurigaku Zasshi Section Abstract Doc Link 9503417 Disease Relevance 0 Pain Relevance 0.19
The slow Ca2+ mobilization was blocked by lower concentrations of competitive nAChR antagonists which did not affect the fast Ca2+ transients.
Negative_regulation (blocked) of Localization (mobilization) of Ca2 associated with antagonist
11) Confidence 0.24 Published 1997 Journal Nippon Yakurigaku Zasshi Section Abstract Doc Link 9503417 Disease Relevance 0 Pain Relevance 0.17
The slow ADP was also reduced by intracellular BAPTA, but it was not blocked by drugs that interfere with Ca2+ release from intracellular stores (CPA, ruthenium red, or heparin).
Negative_regulation (interfere) of Localization (release) of Ca2 in CPA
12) Confidence 0.22 Published 2010 Journal PLoS Biology Section Body Doc Link PMC2982802 Disease Relevance 0 Pain Relevance 0.13
The inhibitory effects of ANP on myocyte Ca2+ responses to Ang II are mediated by GC-A/cGMP/PKG I-dependent modulation of RGS2
Negative_regulation (effects) of Localization (responses) of Ca2 in myocyte
13) Confidence 0.21 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0 Pain Relevance 0
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).
Negative_regulation (reduced) of Localization (release) of Ca2 in platelet associated with agonist
14) Confidence 0.21 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2442636 Disease Relevance 0 Pain Relevance 0.08
Furthermore, inhibition of mitochondrial Ca2+ uptake by low concentrations of FCCP inhibit both cytochrome c release and cell death without preventing A?
Negative_regulation (inhibition) of Localization (uptake) of Ca2 associated with death
15) Confidence 0.18 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2447871 Disease Relevance 0.62 Pain Relevance 0
We show here that, at very low concentrations (1 µM), NSAIDs depolarize mitochondria to the same extent than low concentrations of FCCP, inhibit mitochondrial Ca2+ overload induced by A?
Negative_regulation (inhibit) of Localization (overload) of Ca2 associated with cinod
16) Confidence 0.18 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2447871 Disease Relevance 0.67 Pain Relevance 0.71
These results indicate that inhibition of mitochondrial Ca2+ overload by a partial mitochondrial depolarization protects against the neurotoxicity induced by A?
Spec (partial) Negative_regulation (inhibition) of Localization (overload) of Ca2 associated with drug induced neurotoxicity
17) Confidence 0.18 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2447871 Disease Relevance 0.44 Pain Relevance 0
None of the NSAIDs tested including indomethacin, R-flurbiprofen and sulindac sulfide, all tested at 1 µM, produce any change in resting [Ca2+]cyt or prevent the increase in [Ca2+]cyt induced by A?
Negative_regulation (prevent) of Localization (increase) of Ca2 associated with cinod
18) Confidence 0.18 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2447871 Disease Relevance 0 Pain Relevance 0.41
Application of carbachol after prior exposure to caffeine (at a concentration to deplete the internal store) failed to elicit a Ca2+ transient, whereas pretreatment with carbachol did not prevent further Ca2+ release by caffeine.
Negative_regulation (prevent) of Localization (release) of Ca2 in internal
19) Confidence 0.18 Published 2008 Journal American Journal of Physiology - Renal Physiology Section Body Doc Link PMC2640952 Disease Relevance 0.07 Pain Relevance 0.03
Unlike
               the observation from cardiomyocyte mechanical assessment, the obesity-induced
               decline in intracellular Ca2+ release was further accentuated
               with aging, indicating a possible change in myofilament Ca2+
               sensitivity in the aging ob/ob murine cardiomyocytes. 
Negative_regulation (decline) of Localization (release) of Ca2 in cardiomyocytes associated with aging and obesity
20) Confidence 0.14 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2852499 Disease Relevance 1.13 Pain Relevance 0

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