INT147898

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Context Info
Confidence 0.37
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 16
Total Number 16
Disease Relevance 4.01
Pain Relevance 4.87

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)
Anatomy Link Frequency
Shank 1
Camk2a (Mus musculus)
Pain Link Frequency Relevance Heat
nMDA receptor 19 100.00 Very High Very High Very High
addiction 144 99.56 Very High Very High Very High
opioid receptor 94 99.52 Very High Very High Very High
Morphine 124 99.12 Very High Very High Very High
Neuropathic pain 34 98.60 Very High Very High Very High
Lasting pain 13 98.44 Very High Very High Very High
Spinal cord 42 97.72 Very High Very High Very High
Opioid 17 97.60 Very High Very High Very High
mu opioid receptor 10 95.88 Very High Very High Very High
Intracerebroventricular 5 92.64 High High
Disease Link Frequency Relevance Heat
Morphine Dependence 27 99.56 Very High Very High Very High
Neuropathic Pain 59 98.60 Very High Very High Very High
Pain 34 98.00 Very High Very High Very High
Cognitive Disorder 3 96.56 Very High Very High Very High
Targeted Disruption 135 94.24 High High
Ganglion Cysts 93 93.52 High High
Injury 30 87.60 High High
Nociception 20 86.40 High High
Hyperalgesia 49 86.00 High High
Attention Deficit Hyperactivity Disorder 1 83.32 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The present results provide strong evidence that enhancing the activity of NMDA receptors or CaMKII does not have the same consequence on persistent pain despite being equally implicated in learning-related synaptic plasticity and behavioral memory.
CaMKII Binding (activity) of associated with pain, lasting pain and nmda receptor
1) Confidence 0.37 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 1.16 Pain Relevance 0.29
Indeed, alteration of the affinity of CaMKII and Ca2+/CaM significantly affected the Ca2+-mediated CaMKII activation (see Supplementary information).
CaMKII Binding (affinity) of
2) Confidence 0.36 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Moreover, activated Ca2+/calmodulin-dependent protein kinase II (CaMKII) accumulated in the MOR environment and phosphorylated PhLPl was seen to co-precipitate with these opioid receptors.
CaMKII Binding (co-precipitate) of associated with opioid receptor
3) Confidence 0.35 Published 2008 Journal Neuropharmacology Section Abstract Doc Link 18006024 Disease Relevance 0 Pain Relevance 0.74
Moreover, activated Ca2+/calmodulin-dependent protein kinase II (CaMKII) accumulated in the MOR environment and phosphorylated PhLPl was seen to co-precipitate with these opioid receptors.
calmodulin-dependent protein kinase II Binding (co-precipitate) of associated with opioid receptor
4) Confidence 0.31 Published 2008 Journal Neuropharmacology Section Abstract Doc Link 18006024 Disease Relevance 0 Pain Relevance 0.75
In the following we compare three types of transgene combinations in littermates derived from crosses of mice heterozygous for the transgene CaMKII-tTA and heterozygous for pBEG.
CaMKII Binding (crosses) of
5) Confidence 0.27 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.49 Pain Relevance 0.17
Indeed, the CaMKII?
CaMKII Binding (Indeed) of
6) Confidence 0.27 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.30 Pain Relevance 0.24
Indeed, these changes are associated with the activating Thr286 autophosphorylation of CaMKII.
CaMKII Binding (associated) of
7) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2890584 Disease Relevance 0 Pain Relevance 1.23
The Ca2+/CaMKII protein can phosphorylate (activate) cyclic AMP related element binding (CREB), which leads to increases in c-Fos mRNA and c-Fos protein expression [63].
CaMKII Binding (binding) of
8) Confidence 0.25 Published 2008 Journal Mol Pain Section Body Doc Link PMC2605438 Disease Relevance 1.11 Pain Relevance 1.28
CaMKII (M16112), forward primer 5?
CaMKII Binding (primer) of
9) Confidence 0.21 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0.05 Pain Relevance 0
Further, because decreasing Ca2+ flux through open channels has little effect on Ca2+/CaM elevations, local CaMKII activation is largely dictated by the frequency of channel openings and not the magnitude of the open channel Ca2+ flux, thus accounting for the dichotomous dependences of pCaMKII on Po and iCa (Fig. 5 D).
pCaMKII Binding (accounting) of
10) Confidence 0.21 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0 Pain Relevance 0.06
CaMKII binding to CaV1.2 (Hudmon et al., 2005) generalize to other kinase and channel isoforms.


CaMKII Binding (generalize) of
11) Confidence 0.21 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0.09 Pain Relevance 0.05
Fourth, pCaMKII formation was much more sensitive to changing Po than iCa, thus accounting for the disparate effects on signaling to CREB.
pCaMKII Binding (formation) of
12) Confidence 0.21 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0 Pain Relevance 0.04
Importantly, CaMKII knockdown dramatically reduced pCaMKII puncta formation upon K+ stimulation (Fig. 6 D).
pCaMKII Binding (formation) of
13) Confidence 0.20 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0 Pain Relevance 0
Further structural information on the L-type channel–CaMKII interaction will help clarify whether a direct interaction is necessary for signaling to CREB.
CaMKII Binding (interaction) of
14) Confidence 0.20 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0.08 Pain Relevance 0.03
However, several prominent structural molecules that bind to PSD-95 directly or indirectly, including GKAP, Shank, and CaMKII, are developmentally regulated [75–78].
CaMKII Binding (bind) of in Shank
15) Confidence 0.16 Published 2006 Journal PLoS Biology Section Body Doc Link PMC1634879 Disease Relevance 0 Pain Relevance 0
The Vglut2flox/flox;CamKII-Cre mice showed increased dominance but also increased interaction with their counterparts.
CamKII-Cre Binding (interaction) of
16) Confidence 0.07 Published 2010 Journal Upsala Journal of Medical Sciences Section Body Doc Link PMC2853350 Disease Relevance 0.71 Pain Relevance 0

General Comments

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