INT132468

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Context Info
Confidence 0.70
First Reported 2001
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 20
Total Number 21
Disease Relevance 2.76
Pain Relevance 6.70

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
spinal 2
retina 2
spinal cord 2
dorsal horn 2
Camk2a (Mus musculus)
Pain Link Frequency Relevance Heat
nMDA receptor 101 100.00 Very High Very High Very High
Morphine 117 99.98 Very High Very High Very High
Spinal cord 40 99.44 Very High Very High Very High
tolerance 56 99.20 Very High Very High Very High
opioid receptor 86 98.92 Very High Very High Very High
Glutamate 46 98.80 Very High Very High Very High
Antinociceptive 17 98.80 Very High Very High Very High
long-term potentiation 116 98.62 Very High Very High Very High
Inflammatory mediators 4 98.08 Very High Very High Very High
Pain 77 96.92 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 85 99.36 Very High Very High Very High
INFLAMMATION 36 97.88 Very High Very High Very High
Pain 91 96.92 Very High Very High Very High
Nociception 40 93.08 High High
Retina Disease 1 90.12 High High
Glaucoma 7 87.44 High High
Hyperalgesia 24 86.88 High High
Cv Unclassified Under Development 11 81.00 Quite High
Disease 48 75.20 Quite High
Anaplastic Astrocytoma 1 74.52 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Morphine induced a significant up-regulation of supraspinal and spinal CaMKII activity in tolerant mice, which was abolished after the pretreatment or acute treatment with trifluoperazine.
Positive_regulation (induced) of Positive_regulation (up-regulation) of CaMKII in spinal associated with morphine
1) Confidence 0.70 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16380209 Disease Relevance 0 Pain Relevance 1.06
We also observed that the larger activation of CaMKII in KI samples was due to the presence of mutated CaV2.1 channel activity, because pretreatment with ?
Positive_regulation (due) of Positive_regulation (activation) of CaMKII
2) Confidence 0.53 Published 2010 Journal Mol Pain Section Body Doc Link PMC2940876 Disease Relevance 0 Pain Relevance 0
To establish a sustained CaMKII activation, a [Ca2+]i increase larger than 0.6 ?
Positive_regulation (increase) of Positive_regulation (activation) of CaMKII
3) Confidence 0.49 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
When the duration of conditioning stimulation was shorter, a slightly larger [Ca2+]i increase was required for triggering sustained CaMKII activation (0.6 ?
Positive_regulation (triggering) of Positive_regulation (activation) of CaMKII
4) Confidence 0.49 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
To establish a sustained CaMKII activation, a [Ca2+]i increase larger than 0.6 ?
Positive_regulation (sustained) of Positive_regulation (activation) of CaMKII
5) Confidence 0.49 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
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.
Positive_regulation (increased) of Positive_regulation (increased) of pCaMK-IIalpha in dorsal horn associated with spinal dorsal horn and spinal cord
6) Confidence 0.48 Published 2006 Journal Brain Res. Section Abstract Doc Link 16863646 Disease Relevance 0.27 Pain Relevance 0.40
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.
Positive_regulation (activated) of Positive_regulation (accumulated) of CaMKII associated with opioid receptor
7) Confidence 0.47 Published 2008 Journal Neuropharmacology Section Abstract Doc Link 18006024 Disease Relevance 0 Pain Relevance 0.72
Furthermore, biochemical experiments showed that calcium-dependent CaMKII activity was increased by 2.6 fold in transgenic mice compared to wild-type mice.
Positive_regulation (increased) of Positive_regulation (dependent) of CaMKII associated with targeted disruption
8) Confidence 0.47 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.87 Pain Relevance 0.19
Using the simulation model, we tried to clarify whether each positive-feedback loop contributes to sustained CaMKII activation.
Spec (whether) Positive_regulation (contributes) of Spec (whether) Positive_regulation (activation) of CaMKII
9) Confidence 0.46 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
The computational simulation showed that a transient [Ca2+]i increase induced long-term activation of CaMKII, which was suppressed by GABABR activation coupled with the [Ca2+]i increase.
Positive_regulation (induced) of Positive_regulation (activation) of CaMKII
10) Confidence 0.46 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
To examine this issue, we investigated how large an increase in [Ca2+]i is required to induce sustained CaMKII activation by systematically altering the amplitude of transient [Ca2+]i increase (from 0.1 to 1 ?
Positive_regulation (induce) of Positive_regulation (activation) of CaMKII
11) Confidence 0.46 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Thus, both of the positive-feedback pathways were required for the maintenance of CaMKII activity.
Positive_regulation (required) of Positive_regulation (maintenance) of CaMKII
12) Confidence 0.46 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Some types of synaptic plasticity, such as LTP, require activation of the NMDA receptor, postsynaptic Ca2+ ion influx with concomitant activation of CaMKII [63].
Positive_regulation (activation) of Positive_regulation (activation) of CaMKII associated with nmda receptor
13) Confidence 0.43 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC32198 Disease Relevance 0 Pain Relevance 0.14
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.
Positive_regulation (activated) of Positive_regulation (accumulated) of calmodulin-dependent protein kinase II associated with opioid receptor
14) Confidence 0.41 Published 2008 Journal Neuropharmacology Section Abstract Doc Link 18006024 Disease Relevance 0 Pain Relevance 0.72
Furthermore, autophosphorylation and persistent activation of CaMKII increase steeply with the frequency of Ca2+ pulses (De Koninck and Schulman, 1998).
Positive_regulation (increase) of Positive_regulation (activation) of CaMKII
15) Confidence 0.39 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0 Pain Relevance 0
HFS induced LTP within 5 min and lasts for 3–8 h during the period of recording and resulted in upregulation of p-CaMKII, p-ERK and p-CREB protein levels in the spinal cord and expression of c-Fos in DH.
Positive_regulation (resulted) of Positive_regulation (upregulation) of CaMKII in spinal cord associated with spinal dorsal horn, long-term potentiation and spinal cord
16) Confidence 0.34 Published 2009 Journal Mol Pain Section Abstract Doc Link PMC2704201 Disease Relevance 0.05 Pain Relevance 1.13
CaMKII activation was also followed by the phosphorylation of MOR and the transfer of G?
Positive_regulation (followed) of Positive_regulation (activation) of CaMKII associated with opioid receptor
17) Confidence 0.33 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2890584 Disease Relevance 0.05 Pain Relevance 1.07
Second, a single tethered CaM would be insufficient to trigger persistent activation of CaMKII, which has ?
Positive_regulation (trigger) of Positive_regulation (activation) of CaMKII
18) Confidence 0.28 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0 Pain Relevance 0
The inflammatory mediators activate their respective G-protein coupled receptors to initiate secondary messenger pathways resulting in the activation of either PKA [20, 44, 70, 121, 131, 141], PKC [19, 32, 39, 130, 138, 172, 183], MAPK [76, 204], extracellular Ca2+/CaM-dependent kinase II (CaMKII) [83, 149] or Src kinase [77], which phosphorylate TRPV1.
Positive_regulation (resulting) of Positive_regulation (activation) of CaMKII associated with inflammatory mediators
19) Confidence 0.18 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2647151 Disease Relevance 0.85 Pain Relevance 0.79
Additionally, the observed increases in cAMP may result in activation of PKA, whereas increased [Ca2+]i may result in activation of CaMKII.
Positive_regulation (result) of Positive_regulation (activation) of CaMKII
20) Confidence 0.10 Published 2008 Journal Purinergic Signal Section Body Doc Link PMC2583213 Disease Relevance 0.07 Pain Relevance 0.20

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