INT121871

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Context Info
Confidence 0.81
First Reported 2004
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 9
Total Number 12
Disease Relevance 4.67
Pain Relevance 3.84

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
brain 2
nucleus 2
ACC neurons 1
Camk4 (Mus musculus)
Pain Link Frequency Relevance Heat
Anterior cingulate cortex 341 99.78 Very High Very High Very High
mu opioid receptor 1 99.76 Very High Very High Very High
long-term potentiation 352 99.46 Very High Very High Very High
Pain 21 97.80 Very High Very High Very High
Morphine 11 97.52 Very High Very High Very High
analgesia 15 91.32 High High
Hippocampus 41 88.40 High High
nMDA receptor 102 83.60 Quite High
isoflurane 6 82.96 Quite High
Nucleus accumbens 2 78.48 Quite High
Disease Link Frequency Relevance Heat
Shock 48 98.80 Very High Very High Very High
Enzootic Bovine Leukosis 13 98.00 Very High Very High Very High
Targeted Disruption 225 97.96 Very High Very High Very High
Pain 25 97.80 Very High Very High Very High
Stress 38 93.04 High High
Avian Leukosis 2 93.00 High High
Chronic Lymphoid Leukemia 4 91.92 High High
Disease 20 89.12 High High
Htlv Types I And Ii 6 88.32 High High
Spinal Cord Diseases 2 87.16 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Double immunohistochemical staining showed strong colocalization of CaMKIV with mu-opioid receptors.
Localization (colocalization) of CaMKIV associated with mu opioid receptor
1) Confidence 0.81 Published 2005 Journal Neuroreport Section Abstract Doc Link 15931054 Disease Relevance 0 Pain Relevance 0.52
Since our immunohistochemical study revealed that translocation of CaMKIV into the nuclei was markedly larger in the CaMKIV transgenic mice than in the wild-type mice, protein synthesis would be readily caused by LTP induction in the CaMKIV transgenic mice.
Localization (translocation) of CaMKIV associated with targeted disruption and long-term potentiation
2) Confidence 0.80 Published 2010 Journal Mol Brain Section Body Doc Link PMC2949850 Disease Relevance 0.48 Pain Relevance 0.50
The nuclear location of CaMKIV, its ability to phosphorylate CREB and its broad expression throughout forebrains areas suggests that CaMKIV may play an important role in higher brain function.
Localization (location) of CaMKIV in brain
3) Confidence 0.75 Published 2005 Journal Mol Pain Section Body Doc Link PMC1208947 Disease Relevance 0.70 Pain Relevance 0.34
The nuclear location of CaMKIV, its broad distribution in forebrain areas related to pain, attention and emotion, [10,14-18] and its activation of CREB make it an attractive candidate for the processing of higher brain functions.
Localization (location) of CaMKIV in brain associated with pain
4) Confidence 0.75 Published 2005 Journal Mol Pain Section Body Doc Link PMC1079936 Disease Relevance 0.64 Pain Relevance 0.33
Accordingly, it is likely that the LTP induction stimuli readily recruit CaMKIV in membrane compartments, leading to protein synthesis.
Localization (recruit) of CaMKIV associated with long-term potentiation
5) Confidence 0.75 Published 2010 Journal Mol Brain Section Body Doc Link PMC2949850 Disease Relevance 0 Pain Relevance 0.64
The results of confocal fluorescence microscopy further demonstrated that the activated CREB (P-CREB) was colocalized with CaMKIV in nucleus.
Localization (colocalized) of CaMKIV in nucleus
6) Confidence 0.71 Published 2004 Journal Brain Res. Section Abstract Doc Link 15451364 Disease Relevance 0 Pain Relevance 0.63
CaMKIV over-expression and EEG responses to tone, trace interval, and shock
Localization (responses) of CaMKIV associated with shock
7) Confidence 0.66 Published 2010 Journal Mol Brain Section Body Doc Link PMC2888801 Disease Relevance 0.50 Pain Relevance 0
Sections containing ACC were then used for CaMKIV immunoreactivity.
Localization (used) of CaMKIV associated with anterior cingulate cortex
8) Confidence 0.65 Published 2010 Journal Mol Brain Section Body Doc Link PMC2949850 Disease Relevance 0.08 Pain Relevance 0.22
Our biochemical and immunohistochemical studies revealed that CaMKIV was distributed in the membrane, cytosol and nucleus of ACC neurons.
Localization (distributed) of CaMKIV in ACC neurons associated with anterior cingulate cortex
9) Confidence 0.65 Published 2010 Journal Mol Brain Section Body Doc Link PMC2949850 Disease Relevance 0.40 Pain Relevance 0.39
Both PKA and CaMKIV regulate the activation of CREB in the nucleus either through the subunit translocation (in case of PKA) or the entry of CaM (CaMKIV) [28-30].
Localization (translocation) of CaMKIV in nucleus
10) Confidence 0.51 Published 2010 Journal Mol Brain Section Body Doc Link PMC2822766 Disease Relevance 0.30 Pain Relevance 0.27
Similarly, for these exons with both CaRRE 1 and CaRRE 2, mutations in CaRRE 2 restored splicing in the absence of CaMK (Figure 4C, lanes 7 and 9).
Neg (absence) Localization (absence) of CaMK
11) Confidence 0.37 Published 2007 Journal PLoS Biology Section Body Doc Link PMC1790950 Disease Relevance 0.35 Pain Relevance 0
CaMKIV: calmodulin-depend kinase IV
Localization (kinase) of CaMKIV
12) Confidence 0.10 Published 2007 Journal Retrovirology Section Body Doc Link PMC1839114 Disease Relevance 1.22 Pain Relevance 0

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