INT86544

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Context Info
Confidence 0.47
First Reported 2000
Last Reported 2009
Negated 0
Speculated 0
Reported most in Abstract
Documents 20
Total Number 20
Disease Relevance 4.59
Pain Relevance 11.37

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
neurons 3
TNC 3
spinal 1
cerebral cortex 1
spinal cord 1
Camk2a (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Kinase C 47 100.00 Very High Very High Very High
Neurotransmitter 6 100.00 Very High Very High Very High
cerebral cortex 1 100.00 Very High Very High Very High
Thalamus 1 100.00 Very High Very High Very High
anesthesia 9 99.98 Very High Very High Very High
Pain 64 99.62 Very High Very High Very High
qutenza 43 99.62 Very High Very High Very High
Perioperative pain 2 98.82 Very High Very High Very High
Neuronal nitric oxide synthase 1 98.74 Very High Very High Very High
COX2 8 98.68 Very High Very High Very High
Disease Link Frequency Relevance Heat
Nociception 83 99.02 Very High Very High Very High
Post Operative Pain 2 98.82 Very High Very High Very High
Hyperalgesia 44 98.30 Very High Very High Very High
Li-fraumeni Syndrome 34 96.36 Very High Very High Very High
Headache 9 96.20 Very High Very High Very High
Body Weight 1 95.04 Very High Very High Very High
INFLAMMATION 21 94.24 High High
Pain 58 93.52 High High
Nervous System Injury 9 92.28 High High
Irritable Bowel Syndrome /

Irritable Bowel Syndrome Super / Visceral Pain

27 91.20 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
However, changes of alpha-CaMK II gene levels mentioned above were not detected in amygdala or piriform cortex.
Positive_regulation (changes) of alpha-CaMK II in piriform cortex associated with amygdala
1) Confidence 0.47 Published 2008 Journal Neurochem. Res. Section Abstract Doc Link 18408996 Disease Relevance 0.08 Pain Relevance 0.79
Calcium/calmodulin dependent protein kinase II regulates the phosphorylation of cyclic AMP-responsive element-binding protein of spinal cord in rats following noxious stimulation.
Positive_regulation (dependent) of kinase II in spinal cord associated with qutenza and spinal cord
2) Confidence 0.45 Published 2005 Journal Neurosci. Lett. Section Title Doc Link 15631885 Disease Relevance 0 Pain Relevance 0.89
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.
Positive_regulation (causes) of CaM kinase II in cerebral cortex associated with anesthesia, thalamus and cerebral cortex
3) Confidence 0.45 Published 2007 Journal Ann. N. Y. Acad. Sci. Section Abstract Doc Link 18077565 Disease Relevance 0.16 Pain Relevance 0.60
In rats, subcutaneous administration of NTG (10mg/kg) significantly and selectively increases the number of calmodulin-dependent protein kinase II alpha (CamKIIalpha)-immunoreactive neurons in the trigeminal caudal nucleus (TNC) after 4h.
Positive_regulation (increases) of CamKIIalpha in TNC
4) Confidence 0.43 Published 2009 Journal Neurosci. Lett. Section Abstract Doc Link 19121366 Disease Relevance 0.09 Pain Relevance 0.13
Selective inhibition of cyclooxygenase-2 attenuates nitroglycerin-induced calmodulin-dependent protein kinase II alpha in rat trigeminal nucleus caudalis.
Positive_regulation (induced) of calmodulin-dependent protein kinase II alpha in nucleus associated with cox1
5) Confidence 0.43 Published 2009 Journal Neurosci. Lett. Section Title Doc Link 19121366 Disease Relevance 0.10 Pain Relevance 0.43
In rats, subcutaneous administration of NTG (10mg/kg) significantly and selectively increases the number of calmodulin-dependent protein kinase II alpha (CamKIIalpha)-immunoreactive neurons in the trigeminal caudal nucleus (TNC) after 4h.
Positive_regulation (increases) of calmodulin-dependent protein kinase II alpha in TNC
6) Confidence 0.43 Published 2009 Journal Neurosci. Lett. Section Abstract Doc Link 19121366 Disease Relevance 0.09 Pain Relevance 0.13
Four hours after systemic administration of the nitric oxide donor nitroglycerin (10 mg/kg bodyweight, s.c.), the neurons of the rat caudal trigeminal nucleus are activated, the area covered by calcitonin gene-related peptide (CGRP)-immunoreactive fibres is decreased and the neuronal nitric oxide synthase (nNOS)- and the calmodulin-dependent protein kinase II alpha (CamKIIalpha)-immunopositive neurons in the same area are increased.
Positive_regulation (increased) of CamKIIalpha in neurons associated with neuronal nitric oxide synthase and calcitonin gene-related peptide
7) Confidence 0.40 Published 2009 Journal Eur. J. Pharmacol. Section Abstract Doc Link 19744475 Disease Relevance 0.08 Pain Relevance 0.22
Here, we show, using neuronal tracing and postembedding immunogold labeling, that after acute noxious stimulation (hindpaw capsaicin injections), immunolabeling of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and of CaMKII phosphorylated at Thr(286/287) (pCaMKII) are upregulated postsynaptically at synapses established by peptidergic primary afferent fibers in the superficial dorsal horn of intact rats.
Positive_regulation (upregulated) of calmodulin-dependent protein kinase II in dorsal horn associated with qutenza, primary afferent fibers and dorsal horn
8) Confidence 0.38 Published 2006 Journal J. Neurosci. Section Abstract Doc Link 16624940 Disease Relevance 0.25 Pain Relevance 0.61
Phosphorylation and activity of CaM kinase IV as well as CaM kinase II were increased by treatment of neurons either with glutamate or high K(+).
Positive_regulation (increased) of CaM kinase II in neurons associated with glutamate
9) Confidence 0.37 Published 2000 Journal J. Neurosci. Res. Section Abstract Doc Link 10686587 Disease Relevance 0 Pain Relevance 0.30
Recently, it has been shown that intracerebroventricular (i.c.v.) injection of the D-1 DA receptor agonist, SKF-82958, produces an enhanced locomotor-activating effect as well as increased activation of striatal ERK 1/2 MAP kinase, CaM kinase II, CREB, and c-fos in food-restricted (FR) relative to ad libitum fed (AL) rats.
Positive_regulation (activation) of CaM kinase II associated with dopamine, agonist and intracerebroventricular
10) Confidence 0.33 Published 2005 Journal Brain Res. Mol. Brain Res. Section Abstract Doc Link 16257473 Disease Relevance 0.09 Pain Relevance 0.70
The regulation of the DAT in the PC12 cell model was dependent upon activation of Ca(2+)/calmodulin-dependent kinase II.
Positive_regulation (activation) of calmodulin-dependent kinase II
11) Confidence 0.31 Published 2002 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 11907188 Disease Relevance 0 Pain Relevance 0.30
Secondary hyperalgesia in the postoperative pain model is dependent on spinal calcium/calmodulin-dependent protein kinase II alpha activation.
Positive_regulation (activation) of protein kinase II alpha in spinal associated with hyperalgesia and perioperative pain
12) Confidence 0.30 Published 2007 Journal Anesth. Analg. Section Title Doc Link 18042863 Disease Relevance 0.64 Pain Relevance 0.87
Not surprisingly therefore signal transduction involves Ca2+-dependent pathways including activation of protein kinase C, calcium-calmodulin-dependent protein kinase II (CaMKII), protein kinase A (PKA) phospholipase C (PLC), inositoltriphosphate-3 (IP3) receptors, nitric oxide synthase (NOS) and members of the mitogen-activated protein kinase family (MAPK), including extracellular signal-regulated kinase (ERK) (Fig. 2) [8,12,18,34-36].
Positive_regulation (activation) of calcium-calmodulin-dependent protein kinase II associated with kinase c
13) Confidence 0.24 Published 2007 Journal Mol Pain Section Body Doc Link PMC1852298 Disease Relevance 0.08 Pain Relevance 0.62
Additionally, the coordinated phosphorylation of CREB was initiated by the rapid phosphorylation of MAP kinase, as well as other activated protein kinases, such as calcium/calmodulin protein-dependent kinase II (CaM kinase II), protein kinase A and C [6,9,17,22-24].
Positive_regulation (dependent) of kinase II
14) Confidence 0.15 Published 2005 Journal Mol Pain Section Body Doc Link PMC1224868 Disease Relevance 0.09 Pain Relevance 0.55
The results also showed that, contrary to the activatory role of MAP-ERKs and CaM kinase IV, nuclear alphaCaM kinase II was inactivated in parallel with activation of CREB.
Positive_regulation (inactivated) of nuclear alphaCaM kinase II
15) Confidence 0.11 Published 2009 Journal Int. J. Neuropsychopharmacol. Section Abstract Doc Link 19400982 Disease Relevance 0.08 Pain Relevance 0.31
The mechanisms responsible for the increase include upregulation of P2X3 receptors [11], enhancement of trafficking of P2X3 receptors toward the membrane [31] and activation of calmodulin protein kinase II [34].
Positive_regulation (activation) of calmodulin protein kinase II
16) Confidence 0.10 Published 2007 Journal Mol Pain Section Body Doc Link PMC2063498 Disease Relevance 1.16 Pain Relevance 0.59
In synaptic membranes of chronically treated rats we found a marked reduction in the protein-protein interaction between syntaxin 1 and Thr286-phosphorylated alphaCaM kinase II (alpha-calcium/calmodulin-dependent protein kinase II) (an interaction previously proposed to promote neurotransmitter release) and a marked increase in the interaction between syntaxin 1 and Munc-18 (an interaction proposed to reduce neurotransmitter release).
Positive_regulation (increase) of kinase II associated with neurotransmitter
17) Confidence 0.08 Published 2005 Journal J. Neurosci. Section Abstract Doc Link 15800181 Disease Relevance 0.07 Pain Relevance 0.83
We found that the signal transduction pathways causing LFS-induced LTP in vivo include activation of neurokinin 1 and N-methyl-D-aspartate receptors, rise of [Ca2+]i from intracellular stores and via T-type voltage-dependent Ca2+ channels, activation of phospholipase C, protein kinase C and Ca2+-calmodulin dependent kinase II.
Positive_regulation (activation) of calmodulin dependent kinase II associated with kinase c, li-fraumeni syndrome, nmda receptor and long-term potentiation
18) Confidence 0.05 Published 2008 Journal Mol Pain Section Abstract Doc Link PMC2424039 Disease Relevance 0.64 Pain Relevance 1.16
The activation of nociceptive receptors causes a large influx of extracellular calcium into nociceptive neurons; the increased calcium influx, in turn, activates multiple intracellular protein kinase cascades, such as CaM kinase II, PKA, and PKC [36-40].
Positive_regulation (activates) of kinase II in neurons associated with nociception and kinase c
19) Confidence 0.05 Published 2008 Journal Mol Pain Section Body Doc Link PMC2584043 Disease Relevance 0.79 Pain Relevance 0.85
Ca2+ influx activates calcium/calmodulin-dependent protein kinase II (CaMKII), which is required as a critical cellular cascades for NMDA-dependent LTP [11,36].
Positive_regulation (activates) of kinase II associated with long-term potentiation
20) Confidence 0.03 Published 2008 Journal Mol Brain Section Body Doc Link PMC2570668 Disease Relevance 0 Pain Relevance 0.48

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