INT218822

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Context Info
Confidence 0.50
First Reported 2008
Last Reported 2010
Negated 1
Speculated 1
Reported most in Body
Documents 5
Total Number 6
Disease Relevance 0.91
Pain Relevance 2.41

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) cytoplasm (Camk2a)
Camk2a (Mus musculus)
Pain Link Frequency Relevance Heat
long-term potentiation 231 100.00 Very High Very High Very High
opioid receptor 84 100.00 Very High Very High Very High
tolerance 28 98.40 Very High Very High Very High
Spinal cord 58 97.80 Very High Very High Very High
Morphine 77 94.80 High High
Kinase C 53 93.76 High High
spinal dorsal horn 100 88.08 High High
c fibre 56 82.32 Quite High
Glutamate receptor 10 81.88 Quite High
depression 57 81.12 Quite High
Disease Link Frequency Relevance Heat
Targeted Disruption 93 99.48 Very High Very High Very High
Depression 57 81.12 Quite High
Nervous System Injury 2 72.96 Quite High
Neuropathic Pain 6 70.56 Quite High
Hyperalgesia 16 69.60 Quite High
Anxiety Disorder 28 50.00 Quite Low
Pain 19 43.92 Quite Low
Urological Neuroanatomy 18 41.04 Quite Low
Nociception 12 5.00 Very Low Very Low Very Low
Shock 7 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
As the amount of active CaMKII increased, active PP-1 decreased in a manner depending on PDE1 phosphorylation by CaMKII (Figure 5F).
Negative_regulation (decreased) of Phosphorylation (phosphorylation) of CaMKII
1) Confidence 0.50 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
The rate (kcat) of CaMKII autophosphorylation predominantly determined the CaMKII activity.
Spec (determined) Negative_regulation (determined) of Phosphorylation (autophosphorylation) of CaMKII
2) Confidence 0.42 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Targeted mutation of the EphB1 gene successfully prevented development of LTP and suppressed the associated activation (phosphorylation) of CaMKII, ERK, and CREB as well as increased c-Fos expression.
Negative_regulation (suppressed) of Phosphorylation (phosphorylation) of CaMKII associated with long-term potentiation
3) Confidence 0.36 Published 2009 Journal Mol Pain Section Body Doc Link PMC2704201 Disease Relevance 0 Pain Relevance 0.40
Our results here show that targeted mutation of EphB1 receptor can prevent development of LTP and the associated phosphorylation of CaMKII and ERK and CREB and expression of c-Fos in the mouse SC.
Negative_regulation (prevent) of Phosphorylation (phosphorylation) of CaMKII associated with long-term potentiation and spinal cord
4) Confidence 0.36 Published 2009 Journal Mol Pain Section Body Doc Link PMC2704201 Disease Relevance 0.27 Pain Relevance 0.72
Similarly, the inhibition of CaMKII prevents MOR phosphorylation and reduces AMPAR function [80].
Negative_regulation (prevents) of Phosphorylation (phosphorylation) of CaMKII associated with opioid receptor
5) Confidence 0.31 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2890584 Disease Relevance 0 Pain Relevance 1.11
However, phosphorylation of GluR1 at CaMKII/PKC site was not altered in neurabin KO mice (n?
Neg (not) Negative_regulation (altered) of Phosphorylation (phosphorylation) of CaMKII associated with targeted disruption
6) Confidence 0.30 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2169299 Disease Relevance 0.63 Pain Relevance 0.19

General Comments

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