INT125998

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Context Info
Confidence 0.36
First Reported 2005
Last Reported 2008
Negated 0
Speculated 0
Reported most in Abstract
Documents 3
Total Number 3
Disease Relevance 0.89
Pain Relevance 2.67

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

plasma membrane (Camk2a) kinase activity (Camk2a)
Anatomy Link Frequency
cerebral cortex 1
Camk2a (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Thalamus 1 99.24 Very High Very High Very High
cerebral cortex 1 98.90 Very High Very High Very High
Dorsal horn 5 98.12 Very High Very High Very High
Neurotransmitter 3 98.04 Very High Very High Very High
Spinal cord 16 97.64 Very High Very High Very High
anesthesia 5 97.06 Very High Very High Very High
long-term potentiation 45 96.88 Very High Very High Very High
gABA 3 95.00 High High
Glutamate 7 94.48 High High
nMDA receptor 11 93.80 High High
Disease Link Frequency Relevance Heat
Body Weight 1 89.20 High High
Li-fraumeni Syndrome 24 83.12 Quite High
Stress 1 73.48 Quite High
Neuropathic Pain 4 72.88 Quite High
Hyperalgesia 15 72.32 Quite High
Apoptosis 1 57.76 Quite High
Inflammatory Pain 1 50.12 Quite High
Pain 5 12.16 Low Low
Depression 6 5.00 Very Low Very Low Very Low
Nociception 5 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We found that this general anesthesia causes permanent neuronal deletion in the most vulnerable brain regions-the cerebral cortex and the thalamus-while transiently modulating protein levels of synaptophysin, synaptobrevin, amphiphysin, SNAP-25, and CaM kinase II.
CaM kinase II Binding (levels) of in cerebral cortex associated with anesthesia, thalamus and cerebral cortex
1) Confidence 0.36 Published 2007 Journal Ann. N. Y. Acad. Sci. Section Abstract Doc Link 18077565 Disease Relevance 0.15 Pain Relevance 0.53
In synaptic membranes of chronically treated rats we found a marked reduction in the protein-protein interaction between syntaxin 1 and Thr286-phosphorylated alphaCaM kinase II (alpha-calcium/calmodulin-dependent protein kinase II) (an interaction previously proposed to promote neurotransmitter release) and a marked increase in the interaction between syntaxin 1 and Munc-18 (an interaction proposed to reduce neurotransmitter release).
kinase II Binding (interaction) of associated with neurotransmitter
2) Confidence 0.07 Published 2005 Journal J. Neurosci. Section Abstract Doc Link 15800181 Disease Relevance 0.07 Pain Relevance 0.84
A rise in [Ca2+]i may lead to Ca2+ binding to calmodulin, which in turn activates Ca2+-calmodulin dependent kinase II (CaMKII).
calmodulin dependent kinase II Binding (binding) of
3) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2424039 Disease Relevance 0.67 Pain Relevance 1.30

General Comments

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