INT123386

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Context Info
Confidence 0.58
First Reported 2001
Last Reported 2010
Negated 0
Speculated 2
Reported most in Body
Documents 48
Total Number 50
Disease Relevance 12.57
Pain Relevance 23.78

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
visceral 1
dentate gyrus 1
brain 1
cingulate cortex 1
forebrain 1
Camk2a (Mus musculus)
Camk2a - F89G (1)
Pain Link Frequency Relevance Heat
Kinase C 258 100.00 Very High Very High Very High
nMDA receptor 210 100.00 Very High Very High Very High
opioid receptor 344 99.96 Very High Very High Very High
Hippocampus 271 99.92 Very High Very High Very High
Anterior cingulate cortex 136 99.92 Very High Very High Very High
Morphine 355 99.72 Very High Very High Very High
addiction 58 99.48 Very High Very High Very High
tolerance 151 99.38 Very High Very High Very High
Pain 108 99.20 Very High Very High Very High
Opioid 79 99.18 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 461 99.96 Very High Very High Very High
Aids-related Complex 2 99.90 Very High Very High Very High
Cognitive Disorder 40 98.76 Very High Very High Very High
Pain 136 97.84 Very High Very High Very High
Nociception 145 97.72 Very High Very High Very High
Schizophrenia 140 97.32 Very High Very High Very High
Ganglion Cysts 70 96.96 Very High Very High Very High
Injury 265 96.32 Very High Very High Very High
INFLAMMATION 47 95.88 Very High Very High Very High
Neurodegenerative Disease 41 92.80 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Capsaicin treatment also provoked CaMKII activation and pre-treatment with a specific CaMKII inhibitor prevented the GluR1 trafficking.
Negative_regulation (inhibitor) of CaMKII associated with qutenza
1) Confidence 0.58 Published 2004 Journal Pain Section Abstract Doc Link 15561387 Disease Relevance 0.47 Pain Relevance 1.23
The effect of autophosphorylation at Thr286/287 on CaMKII activation peaked rapidly during the [Ca2+]i increase, whereas that of PDE1 inhibition became stronger about 100 s after the [Ca2+]i increase (Figure 5G; Supplementary Figure 4), when the decrease of CaMKII activity was suppressed.
Negative_regulation (decrease) of CaMKII
2) Confidence 0.57 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
In the mutants, the amount of alpha CaMKII was decreased by 20% to 60% in the cingulate cortex, amygdala, and hippocampus, and the amount of phosphorylated beta-CaMKII was increased in the hippocampus, which is probably a compensatory effect.
Negative_regulation (decreased) of CaMKII in amygdala associated with hippocampus and amygdala
3) Confidence 0.57 Published 2008 Journal Mol Brain Section Body Doc Link PMC2562999 Disease Relevance 0.18 Pain Relevance 0.38
The second phase of nociceptive behavior induced by formalin administered either i.t. or intracerebroventricularly (i.c.v.) was attenuated by PD98059 (ERK inhibitor) as well as KN-93(a CaMK-II inhibitor).
Negative_regulation (inhibitor) of CaMK-II associated with nociception
4) Confidence 0.56 Published 2006 Journal Brain Res. Section Abstract Doc Link 16863646 Disease Relevance 0.38 Pain Relevance 0.41
Opioid-induced phosphorylation of PhLPl was impaired by inhibiting the activity of CaMKII and, in these circumstances, the association of PhLPl with Gbetagamma dimers and 14-3-3 proteins was diminished.
Negative_regulation (inhibiting) of CaMKII associated with opioid
5) Confidence 0.55 Published 2008 Journal Neuropharmacology Section Abstract Doc Link 18006024 Disease Relevance 0 Pain Relevance 0.77
Reversal of morphine antinociceptive tolerance and dependence by the acute supraspinal inhibition of Ca(2+)/calmodulin-dependent protein kinase II.
Negative_regulation (inhibition) of calmodulin-dependent protein kinase II associated with pain, addiction, tolerance, antinociceptive and morphine
6) Confidence 0.51 Published 2006 Journal J. Pharmacol. Exp. Ther. Section Title Doc Link 16505162 Disease Relevance 0.05 Pain Relevance 1.69
These data suggested that trifluoperazine was capable of suppressing opioid tolerance, possibly by the mechanism of inhibiting CaMKII.
Negative_regulation (inhibiting) of CaMKII associated with tolerance and opioid
7) Confidence 0.43 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16380209 Disease Relevance 0 Pain Relevance 1.04
CaMKII-F89G activity could be inhibited by noninvasive oral intake of 1NM-PP1 (5 ?
Negative_regulation (inhibited) of CaMKII (F89G)
8) Confidence 0.43 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.15 Pain Relevance 0.16
An acute supraspinal administration of KN93 [2-[N-(2-hydroxyethyl)]-N-(4-methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzylamine)], a CaMKII inhibitor, was able to dose-dependently reverse the already-established antinociceptive tolerance to morphine (p < 0.001 for 15-30 nmol; not significant for 5 nmol).
Negative_regulation (inhibitor) of CaMKII associated with tolerance, antinociceptive and morphine
9) Confidence 0.43 Published 2006 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 16505162 Disease Relevance 0.07 Pain Relevance 1.71
While our results do not show a direct correlation between the loss of synaptic LTD in the ACC and a reduction in behavioral sensitization in CaMKII transgenic mice, we suggest that the enhanced forebrain CaMKII activity reduced behavioral sensitization to peripheral injury and that the synaptic function of CaMKII in cingulate neurons may be one mechanism contributing to this behavioral phenotype.
Negative_regulation (reduction) of CaMKII in forebrain associated with targeted disruption, injury and anterior cingulate cortex
10) Confidence 0.43 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 1.14 Pain Relevance 0.63
By contrast, we found that behavioral sensitization was reduced in CaMKII transgenic mice.
Negative_regulation (reduced) of CaMKII associated with targeted disruption
11) Confidence 0.43 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 1.21 Pain Relevance 0.81
The effect of acute CaMKII inhibition was not limited to the particular experimental model, because KN93 also acutely reversed the established opioid tolerance and dependence in mice treated with morphine (75 mg/pellet/mouse s.c.) for 6 days.
Negative_regulation (inhibition) of CaMKII associated with addiction, tolerance, opioid and morphine
12) Confidence 0.43 Published 2006 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 16505162 Disease Relevance 0.09 Pain Relevance 1.95
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.
Negative_regulation (reduction) of CaMKII in neurons
13) Confidence 0.42 Published 2008 Journal Mol Brain Section Body Doc Link PMC2562999 Disease Relevance 0.95 Pain Relevance 0.04
When either phosphorylation was stopped by altering each kcat to zero at 30 min after the transient [Ca2+]i increase, the CaMKII activity was attenuated to the basal level (Figure 5A).
Negative_regulation (attenuated) of CaMKII
14) Confidence 0.42 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Thus, CaMKII-mediated inhibition of PDE1 was incorporated into the model.
Negative_regulation (inhibition) of CaMKII-mediated
15) Confidence 0.42 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.14
This study clarified that Ca2+/CaM-activated PDE1 constitutes a feedforward inhibitory pathway and controls the [Ca2+]i threshold by suppressing the CaMKII activity through cAMP, PKA, DARPP-32, and PP-1.
Negative_regulation (suppressing) of CaMKII
16) Confidence 0.42 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Thus, the PDE1-mediated feedforward inhibition of CaMKII and the positive-feedback loop consisting of CaMKII-mediated PDE1 inhibition might underlie regulation of the threshold and/or the maintenance of many forms of synaptic plasticity.
Negative_regulation (inhibition) of CaMKII
17) Confidence 0.42 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.09
The rate (kcat) of CaMKII autophosphorylation predominantly determined the CaMKII activity.
Spec (determined) Negative_regulation (determined) of CaMKII
18) Confidence 0.42 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Thus, it is likely that CaMKII-mediated inhibition of PDE1 in turn supports the CaMKII activity.
Negative_regulation (inhibition) of CaMKII-mediated
19) Confidence 0.42 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
A cell-permeable inhibitory peptide of CaMKII (Ant-AIP-II, 50 ?
Negative_regulation (peptide) of CaMKII
20) Confidence 0.42 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.12

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