INT71590

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Context Info
Confidence 0.78
First Reported 1997
Last Reported 2009
Negated 0
Speculated 0
Reported most in Abstract
Documents 17
Total Number 17
Disease Relevance 2.30
Pain Relevance 8.63

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)
Anatomy Link Frequency
brain 3
nucleus 2
hippocampus 2
frontal cortex 2
nervous system 1
Camk2a (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Calcitonin gene-related peptide 8 100.00 Very High Very High Very High
Kinase C 18 99.92 Very High Very High Very High
Hippocampus 47 99.84 Very High Very High Very High
nMDA receptor 2 99.72 Very High Very High Very High
Morphine 64 99.62 Very High Very High Very High
opioid receptor 8 99.58 Very High Very High Very High
COX-2 inhibitor 3 99.44 Very High Very High Very High
Glutamate 3 99.42 Very High Very High Very High
Thalamus 2 99.24 Very High Very High Very High
cerebral cortex 3 98.90 Very High Very High Very High
Disease Link Frequency Relevance Heat
Urological Neuroanatomy 16 99.20 Very High Very High Very High
Nociception 19 98.82 Very High Very High Very High
INFLAMMATION 3 98.08 Very High Very High Very High
Aging 11 94.32 High High
Body Weight 1 89.20 High High
Disease 7 84.76 Quite High
Cognitive Disorder 10 82.92 Quite High
Amyloid Plaque 2 79.96 Quite High
Headache 9 79.16 Quite High
Apoptosis 1 57.76 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Our data showed that repeated, but not single morphine administration, resulted in significant up-regulation of the alpha-CaMK II gene expression in hippocampus and frontal cortex.
Gene_expression (expression) of alpha-CaMK II in frontal cortex associated with urological neuroanatomy, hippocampus and morphine
1) Confidence 0.78 Published 2008 Journal Neurochem. Res. Section Abstract Doc Link 18408996 Disease Relevance 0.10 Pain Relevance 0.65
The effects of acute and chronic morphine treatments on the expression of Ca2+/calmodulin dependent protein kinase II (CaMK II) gene in rat brain were investigated using in situ hybridization histochemistry.
Gene_expression (expression) of CaMK II in brain associated with morphine
2) Confidence 0.78 Published 2008 Journal Neurochem. Res. Section Abstract Doc Link 18408996 Disease Relevance 0.08 Pain Relevance 0.50
Taken together, our data demonstrate that chronic morphine treatment region-specific up-regulates the levels of the alpha-CaMK II gene expression in hippocampus and frontal cortex.
Gene_expression (expression) of alpha-CaMK II in frontal cortex associated with urological neuroanatomy, hippocampus and morphine
3) Confidence 0.78 Published 2008 Journal Neurochem. Res. Section Abstract Doc Link 18408996 Disease Relevance 0.17 Pain Relevance 0.75
We further studied the time courses of alpha-CaMK II gene expression in response to repeated morphine administration.
Gene_expression (expression) of alpha-CaMK II associated with morphine
4) Confidence 0.78 Published 2008 Journal Neurochem. Res. Section Abstract Doc Link 18408996 Disease Relevance 0.10 Pain Relevance 0.73
Chronic, but not acute morphine treatment, up-regulates alpha-Ca2+/calmodulin dependent protein kinase II gene expression in rat brain.
Gene_expression (expression) of calmodulin dependent protein kinase II in brain associated with morphine
5) Confidence 0.78 Published 2008 Journal Neurochem. Res. Section Title Doc Link 18408996 Disease Relevance 0.08 Pain Relevance 0.74
The effects of acute and chronic morphine treatments on the expression of Ca2+/calmodulin dependent protein kinase II (CaMK II) gene in rat brain were investigated using in situ hybridization histochemistry.
Gene_expression (expression) of calmodulin dependent protein kinase II in brain associated with morphine
6) Confidence 0.68 Published 2008 Journal Neurochem. Res. Section Abstract Doc Link 18408996 Disease Relevance 0.08 Pain Relevance 0.50
The aim of our study was to determine if any isoforms of the cyclooxygenase (COX) enzyme might have a role in the NTG-induced increase of CamKIIalpha expression.
Gene_expression (expression) of CamKIIalpha
7) Confidence 0.66 Published 2009 Journal Neurosci. Lett. Section Abstract Doc Link 19121366 Disease Relevance 0.08 Pain Relevance 0.24
In our experiments, we demonstrated that pretreatment with NS398, the selective COX-2 inhibitor attenuated the NTG-induced CamKIIalpha expression in the TNC at doses of 3 and 5mg/kg.
Gene_expression (expression) of CamKIIalpha in TNC associated with cox-2 inhibitor
8) Confidence 0.66 Published 2009 Journal Neurosci. Lett. Section Abstract Doc Link 19121366 Disease Relevance 0.07 Pain Relevance 0.26
These findings suggest that COX-2, but not COX-1 derived metabolites are important factors in the NTG-induced CamKIIalpha expression.
Gene_expression (expression) of CamKIIalpha
9) Confidence 0.66 Published 2009 Journal Neurosci. Lett. Section Abstract Doc Link 19121366 Disease Relevance 0.06 Pain Relevance 0.29
We found that this general anesthesia causes permanent neuronal deletion in the most vulnerable brain regions-the cerebral cortex and the thalamus-while transiently modulating protein levels of synaptophysin, synaptobrevin, amphiphysin, SNAP-25, and CaM kinase II.
Gene_expression (levels) of CaM kinase II in cerebral cortex associated with anesthesia, thalamus and cerebral cortex
10) Confidence 0.59 Published 2007 Journal Ann. N. Y. Acad. Sci. Section Abstract Doc Link 18077565 Disease Relevance 0.15 Pain Relevance 0.53
The data suggest that the changes caused by nitroglycerin in the expressions of CGRP, nNOS and CamKIIalpha can be influenced by probenecid modulating the inflammatory functions in the nervous system.
Gene_expression (expressions) of CamKIIalpha in nervous system associated with inflammation and calcitonin gene-related peptide
11) Confidence 0.52 Published 2009 Journal Eur. J. Pharmacol. Section Abstract Doc Link 19744475 Disease Relevance 0.18 Pain Relevance 0.46
Accordingly, the aim of the present experiments was to examine the effects of probenecid administration on the nitroglycerin-induced expressions of nNOS, CamKIIalpha and CGRP in the rat caudal trigeminal nucleus.
Gene_expression (expressions) of CamKIIalpha in nucleus associated with calcitonin gene-related peptide
12) Confidence 0.52 Published 2009 Journal Eur. J. Pharmacol. Section Abstract Doc Link 19744475 Disease Relevance 0.09 Pain Relevance 0.41
To investigate the role of calcium/calmodulin-dependent protein kinase II (CaM kinase II) on mu-opioid receptor desensitization, we coexpressed rMOR1 and constitutively active CaM kinase II in HEK293 cells.
Gene_expression (coexpressed) of kinase II associated with opioid receptor
13) Confidence 0.48 Published 1997 Journal J. Neurochem. Section Abstract Doc Link 9326307 Disease Relevance 0 Pain Relevance 0.38
Our data showed that repeated, but not single morphine administration, resulted in significant up-regulation of the alpha-CaMK II gene expression in hippocampus and frontal cortex.
Gene_expression (expression) of alpha-CaMK II in hippocampus associated with urological neuroanatomy, hippocampus and morphine
14) Confidence 0.26 Published 2008 Journal Neurochem. Res. Section Abstract Doc Link 18408996 Disease Relevance 0.10 Pain Relevance 0.65
Taken together, our data demonstrate that chronic morphine treatment region-specific up-regulates the levels of the alpha-CaMK II gene expression in hippocampus and frontal cortex.
Gene_expression (expression) of alpha-CaMK II in hippocampus associated with urological neuroanatomy, hippocampus and morphine
15) Confidence 0.26 Published 2008 Journal Neurochem. Res. Section Abstract Doc Link 18408996 Disease Relevance 0.17 Pain Relevance 0.75
This event produces a large influx of calcium into the nociceptive neurons, activating multiple intracellular protein kinase cascades, such as CaM kinase II, PKC, as well as MAP kinase [2,4,6,18,30-34].
Gene_expression (cascades) of kinase II in neurons associated with nociception and kinase c
16) Confidence 0.20 Published 2005 Journal Mol Pain Section Body Doc Link PMC1224868 Disease Relevance 0.37 Pain Relevance 0.63
Microinfusion experiments have shown that glutamate NMDA receptors, calcium and calmodulin-dependent protein kinase II, and protein synthesis in the entorhinal cortex are involved in and required for extinction.
Gene_expression (synthesis) of calmodulin-dependent protein kinase II in cortex associated with glutamate and nmda receptor
17) Confidence 0.18 Published 2008 Journal Neural Plasticity Section Abstract Doc Link PMC2435227 Disease Relevance 0.42 Pain Relevance 0.14

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