INT121988

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Context Info
Confidence 0.59
First Reported 2004
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 8
Total Number 9
Disease Relevance 4.76
Pain Relevance 5.72

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
brain 4
motoneuron 2
cortex 2
Camk2a (Mus musculus)
Pain Link Frequency Relevance Heat
Anterior cingulate cortex 68 100.00 Very High Very High Very High
withdrawal 30 100.00 Very High Very High Very High
narcan 5 100.00 Very High Very High Very High
depression 27 99.98 Very High Very High Very High
nMDA receptor antagonist 5 99.84 Very High Very High Very High
Morphine 155 99.56 Very High Very High Very High
tolerance 56 99.20 Very High Very High Very High
addiction 41 98.64 Very High Very High Very High
Glutamate 24 96.92 Very High Very High Very High
nMDA receptor 27 96.84 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 244 100.00 Very High Very High Very High
Opiate Addiction 4 100.00 Very High Very High Very High
Depression 27 99.98 Very High Very High Very High
Injury 32 99.30 Very High Very High Very High
Nociception 28 99.26 Very High Very High Very High
Death 13 96.56 Very High Very High Very High
Pain 36 95.92 Very High Very High Very High
Schizophrenia 13 95.40 Very High Very High Very High
Nervous System Injury 2 87.96 High High
Apoptosis 23 85.28 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Considering the important roles of CaMKII in neurodevelopment, it is important to confirm that the phenotypic changes found in brain slices and in nociceptive behaviors can be reversed by simply inhibiting the over expression of CaMKII.
Negative_regulation (inhibiting) of Gene_expression (expression) of CaMKII in brain associated with nociception
1) Confidence 0.59 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.93 Pain Relevance 0.46
Why was behavioral sensitization to injury reduced while synaptic depression abolished in the ACC CaMKII transgenic mice?
Negative_regulation (abolished) of Gene_expression (transgenic mice) of CaMKII associated with targeted disruption, depression, injury and anterior cingulate cortex
2) Confidence 0.43 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 1.26 Pain Relevance 0.87
Furthermore, antisense oligonucleotides that specifically decrease the expression of CaMKII attenuate morphine tolerance and dependence [69].
Negative_regulation (decrease) of Gene_expression (expression) of CaMKII associated with addiction, tolerance and morphine
3) Confidence 0.41 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2890584 Disease Relevance 0 Pain Relevance 1.42
The KO mice also showed decreased expression of the NR1, PSD-95, p-CaMKII, and PAK families, and these signaling pathways are known to regulate synaptic structure and function in the developing cortex [43], [44], [45].
Negative_regulation (decreased) of Gene_expression (expression) of p-CaMKII in cortex associated with targeted disruption
4) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2759290 Disease Relevance 0.66 Pain Relevance 0.24
We do not believe that this is a confounding factor in our case since the expression of the CaMKII driven tTA is switched on during P2 and P5 [28-30], while the sensitive period for physiological motoneuron death is between E14 and P3 [27].
Negative_regulation (switched) of Gene_expression (expression) of CaMKII in motoneuron associated with death
5) Confidence 0.31 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 1.14 Pain Relevance 0.04
CaMKII then acted on nNOS Ser847 to produce a sustained reduction in NO levels.
Negative_regulation (reduction) of Neg (NO) Gene_expression (produce) of CaMKII
6) Confidence 0.30 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2890584 Disease Relevance 0.11 Pain Relevance 1.09
The activation of CaMKII and increased expression of c-Fos protein in the brain of animals with naloxone-precipitated withdrawal syndrome are prevented by NMDA receptor antagonists, whereas the increased levels of extracellular glutamate are not prevented by them.
Negative_regulation (prevented) of Gene_expression (expression) of CaMKII in brain associated with glutamate, nmda receptor antagonist, narcan and withdrawal
7) Confidence 0.24 Published 2004 Journal Eur. J. Pharmacol. Section Abstract Doc Link 15464026 Disease Relevance 0.66 Pain Relevance 1.53
Third, decreasing CaMKII levels reduced both the weight of pCaMKII puncta and the strength of CREB signaling.
Negative_regulation (decreasing) of Gene_expression (levels) of CaMKII
8) Confidence 0.24 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0 Pain Relevance 0.04
Third, decreasing CaMKII levels reduced both the weight of pCaMKII puncta and the strength of CREB signaling.
Negative_regulation (reduced) of Gene_expression (levels) of CaMKII
9) Confidence 0.24 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0 Pain Relevance 0.04

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