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Context Info
Confidence 0.36
First Reported 1993
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 4
Total Number 5
Disease Relevance 1.88
Pain Relevance 1.26

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
reticulum 2
neural 2
Car2 (Mus musculus)
Pain Link Frequency Relevance Heat
Kinase C 3 99.96 Very High Very High Very High
Paracetamol 7 99.42 Very High Very High Very High
long-term potentiation 29 99.36 Very High Very High Very High
antagonist 8 97.90 Very High Very High Very High
Delta opioid receptors 2 96.48 Very High Very High Very High
adenocard 2 91.12 High High
agonist 3 75.08 Quite High
opioid receptor 4 75.00 Quite High
Kappa opioid receptor 1 74.76 Quite High
Enkephalin 1 72.96 Quite High
Disease Link Frequency Relevance Heat
Necrosis 3 99.92 Very High Very High Very High
Overdose 1 97.52 Very High Very High Very High
Alzheimer's Dementia 15 96.96 Very High Very High Very High
Death 8 96.86 Very High Very High Very High
Neurodegenerative Disease 3 92.80 High High
Apoptosis 1 86.28 High High
Coronary Artery Disease 1 79.84 Quite High
Myocardial Infarction 1 77.92 Quite High
Neuroblastoma 1 77.68 Quite High
Hypertrophy 1 76.40 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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 Negative_regulation (inactivation) of Ca2 in reticulum
1) Confidence 0.36 Published 2006 Journal Yonsei Medical Journal Section Body Doc Link PMC2687630 Disease Relevance 0.30 Pain Relevance 0.03
The present studies investigate DNA fragmentation as a critical event in toxic cell death by testing whether the Ca(2+)-calmodulin antagonist chlorpromazine and the Ca2+ channel blocker verapamil prevent acetaminophen-induced hepatic necrosis by inhibiting Ca2+ deregulation and DNA damage.
Spec (whether) Negative_regulation (inhibiting) of Negative_regulation (deregulation) of Ca2 associated with necrosis, paracetamol, antagonist and death
2) Confidence 0.28 Published 1993 Journal FASEB J. Section Abstract Doc Link 8462787 Disease Relevance 1.10 Pain Relevance 0.47
The SNC80-induced neural differentiation was also inhibited by treatment with the protein kinase C (PKC) inhibitor, phosphatidylinositol 3-kinase (PI3K) inhibitor, mitogen-activated protein kinase kinase (MEK) inhibitor or Ca2+/calmodulin-dependent protein kinase II (CaMKII) inhibitor.
Negative_regulation (inhibitor) of Negative_regulation (inhibitor) of Ca2 in neural associated with kinase c
3) Confidence 0.22 Published 2006 Journal J. Neurochem. Section Abstract Doc Link 16696856 Disease Relevance 0.22 Pain Relevance 0.56
42.51 The disruptions in Ca2+ signaling are caused not only by A?
Negative_regulation (caused) of Negative_regulation (disruptions) of Ca2
4) Confidence 0.09 Published 2010 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2938309 Disease Relevance 0.27 Pain Relevance 0.20
The previously reported Ca2+ channel blocker IC50 values are: 1 (diltiazem, IC50 = 0.98 ?
Negative_regulation (reported) of Negative_regulation (blocker) of Ca2
5) Confidence 0.08 Published 2008 Journal PLoS Biology Section Body Doc Link PMC2225441 Disease Relevance 0 Pain Relevance 0

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