INT115650

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Context Info
Confidence 0.70
First Reported 2004
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 37
Total Number 37
Disease Relevance 17.68
Pain Relevance 15.73

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
forebrain 14
hypothalamus 8
brain 6
motoneuron 4
neurons 4
Camk2a (Mus musculus)
Pain Link Frequency Relevance Heat
midbrain 1 100.00 Very High Very High Very High
Morphine 48 99.84 Very High Very High Very High
Locus ceruleus 25 99.68 Very High Very High Very High
allodynia 135 99.40 Very High Very High Very High
Spinal cord 133 99.32 Very High Very High Very High
depression 209 99.00 Very High Very High Very High
Anterior cingulate cortex 510 98.84 Very High Very High Very High
Hyperalgesia 72 98.84 Very High Very High Very High
Intracerebroventricular 5 98.44 Very High Very High Very High
narcan 6 98.12 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 891 100.00 Very High Very High Very High
Aids-related Complex 2 100.00 Very High Very High Very High
Urological Neuroanatomy 1 100.00 Very High Very High Very High
Neuropathic Pain 141 99.40 Very High Very High Very High
Schizophrenia 35 99.36 Very High Very High Very High
Nociception 112 99.12 Very High Very High Very High
Depression 209 99.00 Very High Very High Very High
Hyperalgesia 121 98.84 Very High Very High Very High
Injury 216 97.92 Very High Very High Very High
Opiate Addiction 8 97.24 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We then tested if forebrain overexpression of CaMKII affects synaptic LTD in the ACC.
Positive_regulation (overexpression) of Gene_expression (overexpression) of CaMKII in forebrain associated with anterior cingulate cortex
1) Confidence 0.70 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.45 Pain Relevance 0.40
No CaMKII overexpression was detected in the hindbrain or spinal cord [16].
Neg (No) Positive_regulation (overexpression) of Gene_expression (overexpression) of CaMKII in spinal cord associated with spinal cord
2) Confidence 0.70 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.77 Pain Relevance 0.19
We found that forebrain overexpression of CaMKII did not affect basal nociception and behavioral nociceptive responses to subcutaneous injection of formalin.
Positive_regulation (overexpression) of Gene_expression (overexpression) of CaMKII in forebrain associated with nociception
3) Confidence 0.70 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 1.05 Pain Relevance 0.30
Results described above indicate that overexpressing CaMKII in the forebrain causes selective changes in synaptic LTD without causing any obvious anatomical abnormality or change in neuronal excitability.
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of CaMKII in neuronal associated with neuronal excitability
4) Confidence 0.70 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.49 Pain Relevance 0.36
The rescuing effect of 1NM-PP1 in CaMKII transgenic mice provides strong evidence that the electrophysiological and behavioral changes observed in CaMKII transgenic mice are not due to any developmental changes induced by CaMKII overexpression.
Positive_regulation (overexpression) of Gene_expression (overexpression) of CaMKII associated with targeted disruption
5) Confidence 0.70 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 1.16 Pain Relevance 0.32
Increased expression of Ca2+/calmodulin-dependent protein kinase II alpha during chronic morphine exposure.
Positive_regulation (Increased) of Gene_expression (expression) of Ca2+/calmodulin-dependent protein kinase II alpha associated with morphine
6) Confidence 0.65 Published 2004 Journal Neuroscience Section Title Doc Link 14706789 Disease Relevance 0 Pain Relevance 0.98
Transgenic mice that overexpress a calcium independent form of CaMKII in forebrain areas demonstrated a shift of frequency-dependent responses to repetitive stimulation [4].
Positive_regulation (overexpress) of Gene_expression (overexpress) of CaMKII in forebrain associated with targeted disruption
7) Confidence 0.50 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.17 Pain Relevance 0.16
CaMKII overexpression selectively affected the frequency-response relationship of synaptic plasticity in the CA1 region of the hippocampus [16].
Positive_regulation (overexpression) of Gene_expression (overexpression) of CaMKII in hippocampus associated with hippocampus
8) Confidence 0.50 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.62 Pain Relevance 0.32
CaMKII overexpression did not cause changes in the intrinsic neuronal electrophysiological properties of ACC neurons.
Positive_regulation (overexpression) of Gene_expression (overexpression) of CaMKII associated with anterior cingulate cortex
9) Confidence 0.50 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.55 Pain Relevance 0.35
The rescuing effect of 1NM-PP1 in CaMKII transgenic mice provides strong evidence that the electrophysiological and behavioral changes observed in CaMKII transgenic mice are not due to any developmental changes induced by CaMKII overexpression.
Positive_regulation (transgenic mice) of Gene_expression (transgenic mice) of CaMKII associated with targeted disruption
10) Confidence 0.50 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 1.21 Pain Relevance 0.39
This sustained decrease of PDE1 activity was caused by CaMKII-mediated reduction of the affinity of PDE1 for Ca2+/CaM, as described below.
Positive_regulation (caused) of Gene_expression (reduction) of CaMKII-mediated
11) Confidence 0.49 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.06
In the absence of PDE1, the [Ca2+]i increase required for triggering sustained CaMKII activation (>1 ?
Positive_regulation (triggering) of Gene_expression (activation) of CaMKII
12) Confidence 0.49 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
To test whether sustained activation of CaMKII takes place in living Purkinje neurons, we stained active CaMKII autophosphorylated at Thr286 (in the ?
Positive_regulation (stained) of Gene_expression (stained) of CaMKII in neurons
13) Confidence 0.49 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.07
We found that 1NM-PP1 treatment completely blocked the effects of CaMKII overexpression on behavioral allodynia and hyperalgesia in transgenic mice (n = 4–6 mice, see Fig. 6A and 6B, respectively). 1NM-PP1 treatment alone did not significantly affected hindpaw mechanical withdrawal thresholds (n = 6 mice).
Positive_regulation (overexpression) of Gene_expression (overexpression) of CaMKII associated with targeted disruption, hyperalgesia, allodynia and withdrawal
14) Confidence 0.47 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 1.32 Pain Relevance 0.62
CaMKII overexpression also inhibited synaptic depression induced by a prolonged repetitive stimulation in the ACC, suggesting an important role for CaMKII in the regulation of cingulate neurons.
Positive_regulation (overexpression) of Gene_expression (overexpression) of CaMKII in neurons associated with depression
15) Confidence 0.47 Published 2006 Journal Mol Pain Section Abstract Doc Link PMC1513196 Disease Relevance 0.81 Pain Relevance 0.58
Here we show that genetic overexpression of CaMKII in the mouse forebrain selectively inhibits tissue injury-induced behavioral sensitization, including allodynia and hyperalgesia, while behavioral responses to acute noxious stimuli remain intact.
Positive_regulation (overexpression) of Gene_expression (overexpression) of CaMKII in forebrain associated with hyperalgesia, allodynia and injury
16) Confidence 0.47 Published 2006 Journal Mol Pain Section Abstract Doc Link PMC1513196 Disease Relevance 0.83 Pain Relevance 0.60
Forebrain overexpression of CaMKII abolishes cingulate long term depression and reduces mechanical allodynia and thermal hyperalgesia

Activity-dependent synaptic plasticity is known to be important in learning and memory, persistent pain and drug addiction.

Positive_regulation (overexpression) of Gene_expression (overexpression) of CaMKII in Forebrain associated with drug dependence, pain, addiction, allodynia, depression, lasting pain and thermal hyperalgesia
17) Confidence 0.47 Published 2006 Journal Mol Pain Section Title Doc Link PMC1513196 Disease Relevance 0.79 Pain Relevance 0.62
Our results indicate that the forebrain overexpression of CaMKII significantly affected synaptic depression in the ACC in vitro and behavioral sensitization to inflammation in vivo.
Positive_regulation (overexpression) of Gene_expression (overexpression) of CaMKII in forebrain associated with inflammation, depression and anterior cingulate cortex
18) Confidence 0.47 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 1.30 Pain Relevance 0.61
The present study takes advantage of recently developed CaMKII transgenic mice that use genetic and chemical techniques to spatially and temporally restrict the expression of CaMKII [16], We tested if the overexpression of CaMKII in the forebrain affected neuronal properties and synaptic plasticity in the anterior cingulate cortex (ACC), and then carried out behavioral studies to see if responses to peripheral noxious stimuli and tissue injury were affected in forebrain CaMKII overexpressing mice.
Positive_regulation (overexpression) of Gene_expression (overexpression) of CaMKII in forebrain associated with targeted disruption, injury and anterior cingulate cortex
19) Confidence 0.47 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.54 Pain Relevance 0.57
Alpha-CaMKII is expressed postnatally and dramatically increases from day 5 after birth [46,47].
Positive_regulation (increases) of Gene_expression (expressed) of CaMKII
20) Confidence 0.45 Published 2008 Journal Mol Brain Section Body Doc Link PMC2562999 Disease Relevance 0.71 Pain Relevance 0.08

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