INT125526

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Context Info
Confidence 0.58
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 9
Disease Relevance 4.00
Pain Relevance 0.74

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

nucleoplasm (PRKDC) protein modification process (PRKDC) nucleus (PRKDC)
enzyme binding (PRKDC) DNA binding (PRKDC) transcription factor binding (PRKDC)
Anatomy Link Frequency
brain 5
neurons 1
primary somatosensory cortex 1
PRKDC (Homo sapiens)
Pain Link Frequency Relevance Heat
primary somatosensory cortex 2 99.68 Very High Very High Very High
amygdala 462 94.00 High High
Kinase C 4 90.04 High High
nMDA receptor 149 77.92 Quite High
Inflammation 2 72.12 Quite High
Limbic system 24 67.88 Quite High
cINOD 1 66.80 Quite High
imagery 51 61.44 Quite High
withdrawal 51 58.96 Quite High
cytokine 2 25.00 Low Low
Disease Link Frequency Relevance Heat
Syndrome 181 100.00 Very High Very High Very High
Autism 2036 99.12 Very High Very High Very High
Anxiety Disorder 352 97.80 Very High Very High Very High
Infection 7 97.24 Very High Very High Very High
Prostate Cancer 2 78.96 Quite High
Attention Deficit Hyperactivity Disorder 65 76.44 Quite High
Apoptosis 13 72.56 Quite High
INFLAMMATION 2 72.12 Quite High
Cognitive Disorder 247 71.36 Quite High
Blindness 6 31.24 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Western blot analysis with primary cortical neurons expressing mutant Htt showed that protein levels of Ku70 and Ku80 but not of DNA–PKcs transiently increased at day 1, decreased from day 1 to day 6 after infection, and returned to the initial level (Fig. 6, A–C).
Gene_expression (levels) of DNA-PKcs in neurons associated with infection
1) Confidence 0.58 Published 2010 Journal The Journal of Cell Biology Section Body Doc Link PMC2867301 Disease Relevance 0.10 Pain Relevance 0
Expression of constitutively active PKCs induced an increase in NF-kappa B transcriptional activity and NAG-1 protein levels in LNCaP cells.
Gene_expression (Expression) of PKCs
2) Confidence 0.12 Published 2005 Journal J. Biol. Chem. Section Abstract Doc Link 15757899 Disease Relevance 0.44 Pain Relevance 0.26
The specific molecular cascade that drives hyper-functionality in brain microcircuits is not thought to be necessarily the same in different parts of the brain since there may be different ways to produce hyper-functionality in different regions and we therefore propose a common syndrome rather than a common specific molecular cascade, for all brain regions.
Gene_expression (produce) of hyper-functionality in brain associated with syndrome
3) Confidence 0.01 Published 2010 Journal Frontiers in Human Neuroscience Section Body Doc Link PMC3010743 Disease Relevance 0.54 Pain Relevance 0.03
Furthermore, the Intense World Theory is based on empirical evidence demonstrating that hyper-connectivity within minicolumns produces hyper-reactivity and may render these basic processing units overtly sensitive, autonomous and more difficult to control.
Gene_expression (produces) of hyper-reactivity
4) Confidence 0.01 Published 2010 Journal Frontiers in Human Neuroscience Section Body Doc Link PMC3010743 Disease Relevance 0.43 Pain Relevance 0.03
In the brain, this common molecular syndrome is proposed to have a dual effect of causing hyper-reactivity and hyper-plasticity of microcircuits to produce hyper-functionality (Figure 5).
Gene_expression (produce) of hyper-functionality in brain associated with syndrome
5) Confidence 0.01 Published 2010 Journal Frontiers in Human Neuroscience Section Body Doc Link PMC3010743 Disease Relevance 0.45 Pain Relevance 0.03
In the brain, this common molecular syndrome is proposed to have a dual effect of causing hyper-reactivity and hyper-plasticity of microcircuits to produce hyper-functionality (Figure 5).
Gene_expression (produce) of hyper-reactivity in brain associated with syndrome
6) Confidence 0.01 Published 2010 Journal Frontiers in Human Neuroscience Section Body Doc Link PMC3010743 Disease Relevance 0.56 Pain Relevance 0.03
Hyper-reactivity and hyper-plasticity were also found in the primary somatosensory cortex (Rinaldi et al., 2007a).
Gene_expression (found) of hyper-plasticity in primary somatosensory cortex associated with primary somatosensory cortex
7) Confidence 0.01 Published 2007 Journal Frontiers in Neuroscience Section Body Doc Link PMC2518049 Disease Relevance 0.41 Pain Relevance 0.26
The full spectrum of autism may be explained by the varying degrees of expression of the molecular syndrome that drives hyper-reactivity and hyper-plasticity in different brain regions, depending on the precise moment that the developing brain was exposed to a triggering insult, the type of insult, and the presence of any predisposing genes.
Gene_expression (expression) of hyper-plasticity in brain associated with autism and syndrome
8) Confidence 0.01 Published 2007 Journal Frontiers in Neuroscience Section Body Doc Link PMC2518049 Disease Relevance 0.57 Pain Relevance 0.08
In the brain, this common molecular syndrome is proposed to have a dual effect of causing hyper-reactivity and hyper-plasticity of microcircuits to produce hyper-functionality (Figure 5).
Gene_expression (produce) of hyper-plasticity in brain associated with syndrome
9) Confidence 0.01 Published 2010 Journal Frontiers in Human Neuroscience Section Body Doc Link PMC3010743 Disease Relevance 0.50 Pain Relevance 0.03

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