INT118673

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Context Info
Confidence 0.48
First Reported 2004
Last Reported 2010
Negated 7
Speculated 1
Reported most in Body
Documents 12
Total Number 17
Disease Relevance 7.92
Pain Relevance 5.22

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

signal transduction (Camk4) nucleocytoplasmic transport (Camk4) nucleus (Camk4)
kinase activity (Camk4) cytoplasm (Camk4)
Anatomy Link Frequency
shell 1
Camk4 (Mus musculus)
Pain Link Frequency Relevance Heat
nMDA receptor 118 100.00 Very High Very High Very High
fluoxetine 8 99.84 Very High Very High Very High
antidepressant 5 99.62 Very High Very High Very High
Nucleus accumbens 94 99.28 Very High Very High Very High
Anterior cingulate cortex 403 99.08 Very High Very High Very High
Glutamate receptor 8 97.96 Very High Very High Very High
long-term potentiation 437 96.36 Very High Very High Very High
Eae 50 92.48 High High
analgesia 15 89.28 High High
Hippocampus 44 87.96 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 416 100.00 Very High Very High Very High
Anxiety Disorder 289 98.48 Very High Very High Very High
Syndrome 4 96.56 Very High Very High Very High
Schizophrenia 10 96.28 Very High Very High Very High
Repression 135 95.12 Very High Very High Very High
Intellectual Impairment 2 94.80 High High
Urological Neuroanatomy 6 91.68 High High
Stress 36 90.48 High High
Mental Disorders 2 86.68 High High
Drug Dependence 3 85.96 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Furthermore, calcium-CaM regulated protein kinases including CaMKII and CaMKIV are also critical in synaptic plasticity and behavioral memory [19-27].
Regulation (regulated) of CaMKIV
1) Confidence 0.48 Published 2010 Journal Mol Brain Section Body Doc Link PMC2822766 Disease Relevance 0.34 Pain Relevance 0.29
may partially account for the small effect of CaMKIV deficiency on behavioral phenotype.


Regulation (effect) of CaMKIV
2) Confidence 0.45 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2830479 Disease Relevance 0.64 Pain Relevance 0.03
Roles of calcium-stimulated adenylyl cyclase and calmodulin-dependent protein kinase IV in the regulation of FMRP by group I metabotropic glutamate receptors.
Regulation (Roles) of calmodulin-dependent protein kinase IV associated with glutamate receptor
3) Confidence 0.44 Published 2008 Journal J. Neurosci. Section Title Doc Link 18434517 Disease Relevance 0.52 Pain Relevance 0.33
Both AC1 and CaMKIV contribute to the regulation of FMRP by group I mGluRs probably through cAMP response element-binding protein activation.
Regulation (regulation) of CaMKIV
4) Confidence 0.44 Published 2008 Journal J. Neurosci. Section Abstract Doc Link 18434517 Disease Relevance 0.36 Pain Relevance 0.37
Generation of CaMKIV Mutant Mice
Regulation (Generation) of CaMKIV
5) Confidence 0.39 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2830479 Disease Relevance 0.62 Pain Relevance 0
Anisomycin also showed no effect on NMDA receptor-mediated EPSCs in wild-type (n = 8/5 mice) and CaMKIV transgenic mice (n = 9/5 mice) (Fig. 4B and 4D, respectively).
Neg (no) Regulation (effect) of CaMKIV transgenic associated with targeted disruption and nmda receptor
6) Confidence 0.39 Published 2010 Journal Mol Brain Section Body Doc Link PMC2949850 Disease Relevance 0.56 Pain Relevance 0.42
Actinomycin-D also had no effect on NMDA receptor-mediated EPSCs in wild-type (n = 6/3 mice) and CaMKIV transgenic mice (n = 6/3 mice) (Fig. 3B and 3D, respectively).
Neg (no) Regulation (effect) of CaMKIV transgenic associated with targeted disruption and nmda receptor
7) Confidence 0.39 Published 2010 Journal Mol Brain Section Body Doc Link PMC2949850 Disease Relevance 0.40 Pain Relevance 0.45
Similar to the effect of actinomycin-D, anisomycin had almost no effect on AMPA receptor-mediated EPSCs in wild-type (n = 8/5 mice) and CaMKIV transgenic mice (n = 8/5 mice) (Fig. 4A and 4C, respectively).
Neg (no) Regulation (effect) of CaMKIV transgenic associated with targeted disruption
8) Confidence 0.39 Published 2010 Journal Mol Brain Section Body Doc Link PMC2949850 Disease Relevance 0.52 Pain Relevance 0.46
Actinomycin-D had almost no effect on the AMPA receptor-mediated EPSCs in the wild-type (n = 8/4 mice) and CaMKIV transgenic mice (n = 7/4 mice) (Fig. 3A and 3C, respectively).
Neg (no) Regulation (effect) of CaMKIV transgenic associated with targeted disruption
9) Confidence 0.39 Published 2010 Journal Mol Brain Section Body Doc Link PMC2949850 Disease Relevance 0.42 Pain Relevance 0.41
Next, the response of dnCaMKIV expressing animals on emotional stimuli was investigated in a battery of behavioural tests.


Spec (investigated) Regulation (response) of dnCaMKIV
10) Confidence 0.39 Published 2007 Journal BMC Neurosci Section Body Doc Link PMC2219998 Disease Relevance 0.07 Pain Relevance 0.45
In contrast, disruption of the G track had no effect on CaMK IV response.
Neg (no) Regulation (effect) of CaMK IV
11) Confidence 0.31 Published 2007 Journal PLoS Biology Section Body Doc Link PMC1790950 Disease Relevance 0.50 Pain Relevance 0
However, the CaMK IV response was not affected by this mutation, because the exon was still more excluded in the presence of the activated CaMK IV.
Neg (not) Regulation (affected) of CaMK IV
12) Confidence 0.31 Published 2007 Journal PLoS Biology Section Body Doc Link PMC1790950 Disease Relevance 0.42 Pain Relevance 0
An obvious increased expression of CaMKIV immunoreactivity in the nuclei was observed in CaMKIV transgenic mice (nuclei/cytosolic ratio of CaMKIV staining fluorescence intensity, 0.58 ± 0.02 in wild-type and 1.06 ± 0.03 in CaMKIV transgenic mice, P < 0.001).


Regulation (immunoreactivity) of CaMKIV associated with targeted disruption
13) Confidence 0.27 Published 2010 Journal Mol Brain Section Body Doc Link PMC2949850 Disease Relevance 0.74 Pain Relevance 0.30
The studies addressing anxiety-related behaviour in relation to activity-dependent gene expression in the NAc focused on specific alterations mediated by manipulations of the NAc shell [9-11], while in the present study we targeted CaMKIV activity in both NAc core and shell.
Regulation (targeted) of CaMKIV in shell associated with nucleus accumbens and anxiety disorder
14) Confidence 0.27 Published 2007 Journal BMC Neurosci Section Body Doc Link PMC2219998 Disease Relevance 0.56 Pain Relevance 0.56
Our results show that FLX exerts a more marked effect on CREB phosphorylation and suggest that CaMKIV and MAP kinase cascades are involved in this effect.
Regulation (involved) of CaMKIV associated with fluoxetine
15) Confidence 0.21 Published 2004 Journal Neuropsychopharmacology Section Abstract Doc Link 15138445 Disease Relevance 0.36 Pain Relevance 0.57
This suggests that, as an upstream regulator of CREB, CaMKIV may play a role in the regulation of anxiety-related genes such as oxytocin.
Regulation (regulator) of CaMKIV associated with anxiety disorder
16) Confidence 0.12 Published 2005 Journal Mol Pain Section Body Doc Link PMC1208947 Disease Relevance 0.79 Pain Relevance 0.34
Mood stabilizers such as lithium and valproic acid or the antidepressant fluoxetine had no effect on CaMKIV, CaMKKalpha, CaMKKbeta and calcineurin with the exception of an increase in CaMKKbeta following lithium treatment.
Neg (no) Regulation (effect) of CaMKIV associated with antidepressant and fluoxetine
17) Confidence 0.03 Published 2009 Journal Neuroscience Section Abstract Doc Link 19289156 Disease Relevance 0.10 Pain Relevance 0.24

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