INT119528

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Context Info
Confidence 0.70
First Reported 2001
Last Reported 2010
Negated 3
Speculated 3
Reported most in Body
Documents 135
Total Number 147
Disease Relevance 26.13
Pain Relevance 54.70

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
neurons 9
brain 6
forebrain 5
retina 4
spinal 2
Camk2a (Mus musculus)
Pain Link Frequency Relevance Heat
nMDA receptor 605 100.00 Very High Very High Very High
Kinase C 587 100.00 Very High Very High Very High
midbrain 32 100.00 Very High Very High Very High
tolerance 339 99.96 Very High Very High Very High
addiction 256 99.92 Very High Very High Very High
long-term potentiation 1414 99.90 Very High Very High Very High
Morphine 820 99.84 Very High Very High Very High
Opioid 175 99.84 Very High Very High Very High
antidepressant 139 99.78 Very High Very High Very High
Hippocampus 341 99.68 Very High Very High Very High
Disease Link Frequency Relevance Heat
Ganglion Cysts 297 100.00 Very High Very High Very High
Urological Neuroanatomy 171 100.00 Very High Very High Very High
Targeted Disruption 967 99.96 Very High Very High Very High
Schizophrenia 159 99.36 Very High Very High Very High
Hypertrophy 16 99.32 Very High Very High Very High
Neurodegenerative Disease 68 99.18 Very High Very High Very High
Injury 418 98.84 Very High Very High Very High
Neuropathic Pain 163 98.72 Very High Very High Very High
Pain 581 98.00 Very High Very High Very High
INFLAMMATION 156 97.54 Very High Very High Very 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 (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
These results provide evidence that the increase in CaMKII activity in the mouse limbic forebrain may contribute to the rewarding effect, but not the antinociception and the hyperlocomotion, induced by morphine.
Positive_regulation (increase) of CaMKII in forebrain associated with antinociception and morphine
2) Confidence 0.70 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207359 Disease Relevance 0.08 Pain Relevance 1.01
However, the enhanced activity of CaMKII would tonically alter the signaling pathways within neurons, including a disruption of normal function and expression of NMDA receptors in the forebrain.
Positive_regulation (enhanced) of CaMKII in neurons associated with nmda receptor
3) Confidence 0.70 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 1.08 Pain Relevance 0.56
We found that behavioral responses to noxious thermal stimuli were similar between wild-type and transgenic mice (Fig. 4, tail-flick test: wild-type, n = 6 mice; transgenic mice, n = 7 mice; thermal withdrawal: wild-type, n = 10 mice, transgenic mice, n = 6 mice), indicating that enhanced CaMKII activity in the forebrain did not significantly affect acute behavioral responses to noxious stimuli.
Positive_regulation (enhanced) of CaMKII in forebrain associated with targeted disruption, tail-flick and withdrawal
4) Confidence 0.70 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.75 Pain Relevance 0.27
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.
Positive_regulation (enhanced) of CaMKII in neurons associated with targeted disruption, injury and anterior cingulate cortex
5) Confidence 0.70 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 1.16 Pain Relevance 0.61
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 (dependent) of CaMKII associated with targeted disruption
6) Confidence 0.70 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.86 Pain Relevance 0.19
These results consistently demonstrate that behavioral responses to acute noxious thermal and mechanical stimuli were not affected by enhanced forebrain CaMKII activity.
Positive_regulation (enhanced) of CaMKII in forebrain
7) Confidence 0.70 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.93 Pain Relevance 0.39
CaMKII activity was increased after the treatment with morphine (100 mg/kg s.c. or 75 mg s.c. of morphine/pellet/mouse); the effect exhibited a temporal correction with the development of opioid tolerance and dependence.
Positive_regulation (increased) of CaMKII associated with addiction, tolerance, opioid and morphine
8) Confidence 0.70 Published 2006 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 16505162 Disease Relevance 0 Pain Relevance 1.31
Capsaicin treatment also provoked CaMKII activation and pre-treatment with a specific CaMKII inhibitor prevented the GluR1 trafficking.
Positive_regulation (activation) of CaMKII associated with qutenza
9) Confidence 0.69 Published 2004 Journal Pain Section Abstract Doc Link 15561387 Disease Relevance 0.47 Pain Relevance 1.23
Long-term activation of CaMKII in living Purkinje neurons
Positive_regulation (activation) of CaMKII in neurons
10) Confidence 0.68 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.06
To test whether sustained activation of CaMKII takes place in living Purkinje neurons, we stained active CaMKII autophosphorylated at Thr286 (in the ?
Spec (whether) Positive_regulation (activation) of CaMKII in neurons
11) Confidence 0.68 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.07
Next, we examined the effect of varying kcat of each phosphorylation on CaMKII activation in response to the transient [Ca2+]i increase (Figure 5C and D).
Positive_regulation (activation) of CaMKII
12) Confidence 0.68 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 (activation) of CaMKII
13) Confidence 0.68 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 (activation) of CaMKII
14) Confidence 0.68 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Activation of Ca2+/calmodulin dependent protein kinase II (CaMKII) and protein kinase C (PKC) are hallmarks of opioid tolerance and dependence.
Positive_regulation (Activation) of CaMKII associated with addiction, kinase c, tolerance and opioid
15) Confidence 0.68 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16824682 Disease Relevance 0 Pain Relevance 0.84
Alpha-CaMKII is expressed postnatally and dramatically increases from day 5 after birth [46,47].
Positive_regulation (increases) of CaMKII
16) Confidence 0.68 Published 2008 Journal Mol Brain Section Body Doc Link PMC2562999 Disease Relevance 0.71 Pain Relevance 0.08
At the supraspinal level, although pERK was not changed in the hippocampus induced by formalin s.c. injection, pCaMK-IIalpha was increased in the hippocampus and hypothalamus by s.c. formalin injection, and an increase of pCaMK-IIalpha immunoreactivity mainly occurred in the pyramidal cells and the stratum lucidum/radiatum layer of the CA3 region of hippocampus and paraventricular nucleus of the hypothalamus.
Positive_regulation (increased) of pCaMK-IIalpha in hypothalamus associated with pyramidal cell and hippocampus
17) Confidence 0.66 Published 2006 Journal Brain Res. Section Abstract Doc Link 16863646 Disease Relevance 0.36 Pain Relevance 0.44
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 pCaMK-IIalpha in dorsal horn associated with spinal dorsal horn and spinal cord
18) Confidence 0.66 Published 2006 Journal Brain Res. Section Abstract Doc Link 16863646 Disease Relevance 0.27 Pain Relevance 0.40
Antisense-pretreated mice showed decreased neurogranin expression, lack of morphine-induced phosphorylation of neurogranin and activation of CaMKII and CREB, and absence of naloxone-induced withdrawal jumping.
Positive_regulation (activation) of CaMKII associated with narcan, withdrawal and morphine
19) Confidence 0.66 Published 2007 Journal Brain Res. Section Abstract Doc Link 17306231 Disease Relevance 0.16 Pain Relevance 0.91
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 CaMKII associated with opioid receptor
20) Confidence 0.66 Published 2008 Journal Neuropharmacology Section Abstract Doc Link 18006024 Disease Relevance 0 Pain Relevance 0.72

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