INT119527

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Context Info
Confidence 0.60
First Reported 2004
Last Reported 2010
Negated 3
Speculated 1
Reported most in Body
Documents 26
Total Number 27
Disease Relevance 5.55
Pain Relevance 9.01

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
neurons 3
forebrain 2
synapse 2
hypothalamus 1
Shank 1
Camk2a (Mus musculus)
Pain Link Frequency Relevance Heat
Morphine 166 100.00 Very High Very High Very High
Kinase C 127 100.00 Very High Very High Very High
opioid receptor 169 99.84 Very High Very High Very High
Opioid 40 99.60 Very High Very High Very High
tolerance 63 99.32 Very High Very High Very High
nMDA receptor 138 99.12 Very High Very High Very High
analgesia 9 98.64 Very High Very High Very High
Spinal cord 79 98.56 Very High Very High Very High
depression 115 98.40 Very High Very High Very High
midbrain 8 98.34 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 183 98.86 Very High Very High Very High
Depression 115 98.40 Very High Very High Very High
Hyperalgesia 53 98.28 Very High Very High Very High
Urological Neuroanatomy 42 97.88 Very High Very High Very High
Opiate Addiction 3 93.76 High High
Nociception 105 92.08 High High
Pain 97 91.60 High High
Schizophrenia 35 91.28 High High
Injury 45 90.08 High High
Death 13 81.48 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The rate of PDE1 phosphorylation determined the working range within which a change of the CaMKII activity effectively influenced the PP-1 activity.
Regulation (change) of CaMKII
1) Confidence 0.60 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
The levels of phosphorylated-CaMKII (p-CaMKII) in the limbic forebrain, but not in the frontal cortex and the lower midbrain, were significantly increased in morphine-conditioned mice, whereas the levels of CaMKII in three brain regions obtained from morphine-conditioned mice were not changed.
Neg (not) Regulation (changed) of CaMKII in brain associated with urological neuroanatomy, midbrain and morphine
2) Confidence 0.45 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207359 Disease Relevance 0.10 Pain Relevance 1.06
These results consistently demonstrate that behavioral responses to acute noxious thermal and mechanical stimuli were not affected by enhanced forebrain CaMKII activity.
Neg (not) Regulation (affected) of CaMKII in forebrain
3) Confidence 0.45 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.93 Pain Relevance 0.39
While the autophosphorylation and dephosphorylation of CaMKII support the hypothesis that it can act as a "molecular switch" in plasticity and memory, recent studies favor a more sophisticated frequency-dependent biphasic modulation of CaMKII in learning-related synapses.
Regulation (modulation) of CaMKII in synapses
4) Confidence 0.45 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.17 Pain Relevance 0.10
Our results show that delivery of GluR1 AMPA receptor subunits to the cell membrane through a CaMKII activity-dependent exocytotic regulated pathway contributes to the development of hyperalgesia after a painful stimulus.
Regulation (regulated) of CaMKII associated with pain and hyperalgesia
5) Confidence 0.45 Published 2004 Journal Pain Section Abstract Doc Link 15561387 Disease Relevance 0.26 Pain Relevance 1.04
To elucidate the role of PDE1 inhibition by CaMKII, we analyzed how the CaMKII activity affects the PP-1 activity through PDE1 phosphorylation.
Spec (analyzed) Regulation (affects) of CaMKII
6) Confidence 0.44 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Considering the fact that only a 50% reduction of alpha-CaMKII mRNA caused such a dramatic and qualitative change of the nature of the DG neurons, any genetic or environmental alterations affecting CaMKII signaling pathways could result in a similar change or similar endophenotypes.
Regulation (affecting) of CaMKII in neurons
7) Confidence 0.44 Published 2008 Journal Mol Brain Section Body Doc Link PMC2562999 Disease Relevance 0.99 Pain Relevance 0.05
Furthermore, calcium-CaM regulated protein kinases including CaMKII and CaMKIV are also critical in synaptic plasticity and behavioral memory [19-27].
Regulation (regulated) of CaMKII
8) Confidence 0.41 Published 2010 Journal Mol Brain Section Body Doc Link PMC2822766 Disease Relevance 0.34 Pain Relevance 0.29
In addition they carry a transgene in which the Cre recombinase is placed under the control of CaMKII regulatory sequences that are forebrain neuron-specific.
Regulation (control) of CaMKII in neuron
9) Confidence 0.40 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525857 Disease Relevance 0.27 Pain Relevance 0.08
The efficacy of the described treatments in preventing and rescuing morphine analgesia from tolerance can be explained by linking early events with those responsible for sustained NMDAR potentiation and subsequent CaMKII action on MORs.
Regulation (responsible) of CaMKII associated with tolerance, analgesia and morphine
10) Confidence 0.32 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2890584 Disease Relevance 0.06 Pain Relevance 1.05
To further clarify the role of each positive-feedback loop, the effect of altering the strength of each phosphorylation on the CaMKII activity was examined.
Regulation (altering) of CaMKII
11) Confidence 0.26 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
The effect appeared to correlate with the changes in the activities of PKC and CaMKII, and with the development of opioid tolerance and dependence.
Regulation (changes) of CaMKII associated with addiction, kinase c, tolerance and opioid
12) Confidence 0.26 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16824682 Disease Relevance 0 Pain Relevance 1.47
CaMKII was also found to phosphorylate Serine831 in GluR1 and contributes to the single-channel conductance of the receptor and may increase AMPA receptor conductance during LTP [35,40].
Regulation (contributes) of CaMKII
13) Confidence 0.26 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0.14 Pain Relevance 0.21
In the immunoblot assay, subcutaneous (s.c.) injection with formalin increased the pERK and pCaMK-IIalpha level in the spinal cord, and an immunohistochemical study showed that the increase of pERK and pCaMK-IIalpha immunoreactivity mainly occurred in the laminae I and II areas of the spinal dorsal horn.
Regulation (immunoreactivity) of pCaMK-IIalpha in dorsal horn associated with spinal dorsal horn and spinal cord
14) Confidence 0.26 Published 2006 Journal Brain Res. Section Abstract Doc Link 16863646 Disease Relevance 0.31 Pain Relevance 0.42
Neurogranin has been suggested to serve as a common regulator synchronizing the activities of PKC and CaMKII in acute opioid tolerance.
Regulation (regulator) of CaMKII associated with tolerance and opioid
15) Confidence 0.26 Published 2007 Journal Brain Res. Section Abstract Doc Link 17306231 Disease Relevance 0.17 Pain Relevance 0.64
The regulation of kinases such as PKA and CaMKII has been studied in great detail, whereas much less attention has been given to the regulation of phosphatase activity.
Regulation (regulation) of CaMKII
16) Confidence 0.25 Published 2006 Journal PLoS Computational Biology Section Body Doc Link PMC1562452 Disease Relevance 0 Pain Relevance 0.14
By comparison, CaMKII immunoreactivity was detected only in 15 ± 4 and 9 ± 3% of neurons in cultures or intact ganglia from WT mice (n = 3-5; p = 0.03; see example in Fig. 5A).
Regulation (immunoreactivity) of CaMKII in neurons
17) Confidence 0.21 Published 2010 Journal Mol Pain Section Body Doc Link PMC2940876 Disease Relevance 0 Pain Relevance 0
These mice were crossed with mice expressing the Tet-transactivator under control of the CaMKII ?
Regulation (control) of CaMKII
18) Confidence 0.20 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.56 Pain Relevance 0.15
This regulation integrates the positive effects of PI3K, Akt, nNOS, PKC, Src, NMDAR and CaMKII on MOR inhibition.
Regulation (effects) of CaMKII associated with kinase c and opioid receptor
19) Confidence 0.19 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2890584 Disease Relevance 0.07 Pain Relevance 1.00
However, several prominent structural molecules that bind to PSD-95 directly or indirectly, including GKAP, Shank, and CaMKII, are developmentally regulated [75–78].
Regulation (regulated) of CaMKII in Shank
20) Confidence 0.19 Published 2006 Journal PLoS Biology Section Body Doc Link PMC1634879 Disease Relevance 0 Pain Relevance 0

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