INT166435

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Context Info
Confidence 0.43
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 8
Total Number 10
Disease Relevance 0.40
Pain Relevance 0.44

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

transport (Atp2a2) endoplasmic reticulum (Atp2a2) protein complex (Atp2a2)
Anatomy Link Frequency
plasma 1
cardiomyocyte 1
hearts 1
Atp2a2 (Mus musculus)
Pain Link Frequency Relevance Heat
anesthesia 9 86.72 High High
addiction 5 73.52 Quite High
antagonist 3 65.00 Quite High
Potency 2 58.24 Quite High
Catecholamine 3 45.84 Quite Low
ketamine 8 5.00 Very Low Very Low Very Low
Central nervous system 7 5.00 Very Low Very Low Very Low
Calcium channel 7 5.00 Very Low Very Low Very Low
depression 6 5.00 Very Low Very Low Very Low
fibrosis 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Disease 65 92.44 High High
Stress 84 70.16 Quite High
Bacillus Anthracis Infection 84 50.00 Quite Low
Lysosomal Storage Diseases 24 50.00 Quite Low
Hypertrophy 8 49.28 Quite Low
Myocardial Infarction 5 42.08 Quite Low
Heart Rate Under Development 4 36.72 Quite Low
Cognitive Disorder 5 32.40 Quite Low
Toxicity 6 31.88 Quite Low
Pressure Volume 2 Under Development 9 24.76 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To test this hypothesis, we compared VO2max and exercise capacity in mice with cardiac disruption of Serca2 (SERCA2 KO) with control mice (SERCA2 FF).
Negative_regulation (disruption) of SERCA2
1) Confidence 0.43 Published 2010 Journal J. Appl. Physiol. Section Abstract Doc Link 20167673 Disease Relevance 0 Pain Relevance 0.07
To test this hypothesis, we compared VO2max and exercise capacity in mice with cardiac disruption of Serca2 (SERCA2 KO) with control mice (SERCA2 FF).
Negative_regulation (disruption) of Serca2
2) Confidence 0.43 Published 2010 Journal J. Appl. Physiol. Section Abstract Doc Link 20167673 Disease Relevance 0 Pain Relevance 0.07
High-intensity exercise training in mice with cardiomyocyte-specific disruption of Serca2.
Negative_regulation (disruption) of Serca2 in cardiomyocyte
3) Confidence 0.43 Published 2010 Journal J. Appl. Physiol. Section Title Doc Link 20167673 Disease Relevance 0 Pain Relevance 0.07
Hence, a reduction in SERCA2 abundance is expected to reduce work performance and maximal oxygen uptake (VO2max) and to limit the response to exercise training.
Negative_regulation (reduction) of SERCA2
4) Confidence 0.38 Published 2010 Journal J. Appl. Physiol. Section Abstract Doc Link 20167673 Disease Relevance 0 Pain Relevance 0
Treadmill running at 85-90% of VO2max started 2 wk after Serca2 gene disruption and continued for 4 wk.
Negative_regulation (disruption) of Serca2
5) Confidence 0.38 Published 2010 Journal J. Appl. Physiol. Section Abstract Doc Link 20167673 Disease Relevance 0 Pain Relevance 0.09
Our data revealed down-regulation of phospholamban, an endogenous inhibitor of SERCA, in APP/PS1 mouse hearts.
Negative_regulation (inhibitor) of SERCA in hearts
6) Confidence 0.14 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2696039 Disease Relevance 0.23 Pain Relevance 0
To further investigate the idea that diltiazem enhances GC activity by blocking plasma membrane Ca2+ ion channels, thus lowering intracellular Ca2+ concentrations, thapsigargin¬óa potent SERCA inhibitor¬ówas applied to L444P GC cells without or with 10 ?
Negative_regulation (inhibitor) of SERCA in plasma
7) Confidence 0.04 Published 2008 Journal PLoS Biology Section Body Doc Link PMC2225441 Disease Relevance 0 Pain Relevance 0.09
Our results revealed downregulated SERCA in conjunction with upregulated phospholamban, an endogenous inhibitor of SERCA, following in vitro lethal toxin exposure, favoring a likely role of SERCA/phospholamban in lethal toxin-induced intracellular Ca2+ dysregulation.
Negative_regulation (downregulated) of SERCA
8) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954163 Disease Relevance 0.06 Pain Relevance 0.03
Our in vitro data revealed that cellular machineries responsible for cardiac relaxation such as SERCA and phospholamban were downregulated and upregulated, respectively, in response to lethal toxin exposure.
Negative_regulation (downregulated) of SERCA
9) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954163 Disease Relevance 0 Pain Relevance 0
Our results revealed downregulated SERCA in conjunction with upregulated phospholamban, an endogenous inhibitor of SERCA, following in vitro lethal toxin exposure, favoring a likely role of SERCA/phospholamban in lethal toxin-induced intracellular Ca2+ dysregulation.
Negative_regulation (inhibitor) of SERCA
10) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954163 Disease Relevance 0.11 Pain Relevance 0.04

General Comments

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