INT297202

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Context Info
Confidence 0.16
First Reported 2010
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 2
Total Number 5
Disease Relevance 1.71
Pain Relevance 0.14

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
cardiomyocyte 1
Atp2a2 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 4 79.68 Quite High
depression 8 73.52 Quite High
addiction 4 59.04 Quite High
ketamine 8 5.00 Very Low Very Low Very Low
anesthesia 5 5.00 Very Low Very Low Very Low
fibrosis 4 5.00 Very Low Very Low Very Low
cva 4 5.00 Very Low Very Low Very Low
agonist 2 5.00 Very Low Very Low Very Low
isoflurane 1 5.00 Very Low Very Low Very Low
imagery 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Death 31 99.76 Very High Very High Very High
Stress 94 92.96 High High
Infection 47 89.72 High High
Bacillus Anthracis Infection 112 88.80 High High
Arrhythmia Under Development 13 86.80 High High
Heart Rate Under Development 6 80.84 Quite High
INFLAMMATION 4 79.68 Quite High
Depression 8 73.52 Quite High
Pathologic Processes 4 69.52 Quite High
Hypertrophy 6 59.44 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
2-adrenergic receptor but no changes in SERCA2, RyR2, or PLN (Fig. 4B).
Neg (no) Regulation (changes) of SERCA2
1) Confidence 0.16 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2825466 Disease Relevance 0.30 Pain Relevance 0
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.
Regulation (responsible) of SERCA
2) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954163 Disease Relevance 0 Pain Relevance 0
Perhaps the most novel finding from our study was that NADPH oxidase inhibition with apocynin mitigated lethal toxin-induced cardiomyocyte contractile dysfunction, intracellular Ca2+ mishandling, intracellular superoxide generation, cell death as well as change in Ca2+ regulatory proteins SERCA2a and phospholamban.
Regulation (change) of SERCA2a in cardiomyocyte associated with death
3) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954163 Disease Relevance 0.92 Pain Relevance 0.07
SERCA is considered as the single most important machinery to remove Ca2+ from cytosolic space (responsible for 92% Ca2+ removal) for cardiac relaxation to occur [27].
Regulation (responsible) of SERCA
4) Confidence 0.02 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954163 Disease Relevance 0 Pain Relevance 0.03
Ca2+ regulatory proteins SERCA2a and phospholamban were also differentially regulated by in vitro and in vivo lethal toxins.
Regulation (regulated) of SERCA2a
5) Confidence 0.02 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2954163 Disease Relevance 0.49 Pain Relevance 0.04

General Comments

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