INT272360

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Context Info
Confidence 0.61
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 13
Total Number 15
Disease Relevance 4.33
Pain Relevance 0.69

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

mRNA processing (Adar) nucleolus (Adar) RNA binding (Adar)
nucleus (Adar) intracellular (Adar) DNA binding (Adar)
Anatomy Link Frequency
ADAR 4
brain 3
liver 1
neurons 1
Adar (Mus musculus)
Pain Link Frequency Relevance Heat
adenocard 144 94.76 High High
Neuronal excitability 12 87.56 High High
Neurotransmitter 24 74.60 Quite High
Serotonin 168 73.12 Quite High
Glutamate 129 71.80 Quite High
Glutamate receptor 45 66.56 Quite High
depression 36 63.48 Quite High
Central nervous system 42 62.68 Quite High
Action potential 60 45.04 Quite Low
potassium channel 48 44.40 Quite Low
Disease Link Frequency Relevance Heat
Targeted Disruption 90 99.76 Very High Very High Very High
Thiamine Deficiency 186 99.42 Very High Very High Very High
Brain Tumor 24 98.76 Very High Very High Very High
Anaplastic Astrocytoma 36 97.44 Very High Very High Very High
Epilepsy 108 95.76 Very High Very High Very High
Glioblastoma 60 95.00 High High
Malignant Neoplastic Disease 24 94.68 High High
Cancer 108 93.56 High High
Neurodegenerative Disease 24 90.60 High High
Disease 66 87.76 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Two studies tried to establish a correlation between ADAR mRNA expression level and editing frequency of 5-HT2CR and GluR-B transcripts [45,47], but concluded that changes in expression level only is an insufficient model.
Gene_expression (expression) of ADAR mRNA in ADAR
1) Confidence 0.61 Published 2009 Journal Mol Brain Section Body Doc Link PMC2694175 Disease Relevance 0.09 Pain Relevance 0.07
A reduction in RNA editing efficacy is observed in transgenic Drosophila expressing both wild type and inactive ADAR isoforms, which retains the binding to dsRNA substrates [38].
Gene_expression (expressing) of ADAR in ADAR associated with targeted disruption
2) Confidence 0.61 Published 2009 Journal Mol Brain Section Body Doc Link PMC2694175 Disease Relevance 0.19 Pain Relevance 0
Overexpression of ADAR1 and ADAR2 in GBM cell line results in a decreased proliferation rate, suggesting that reduced A-to-I editing in brain tumors is involved in the pathogenesis of cancer [59].
Gene_expression (Overexpression) of ADAR1 in brain associated with cancer and brain tumor
3) Confidence 0.61 Published 2009 Journal Mol Brain Section Body Doc Link PMC2694175 Disease Relevance 1.24 Pain Relevance 0
This review attempts to provide an insight to existing models of explanation – regulation of ADAR expression and activity by self-editing, alternative splicing and cross-talk among ADAR family members; developmental and activity-dependent regulation of A-to-I editing through environmental cues.
Gene_expression (expression) of ADAR in ADAR
4) Confidence 0.61 Published 2009 Journal Mol Brain Section Body Doc Link PMC2694175 Disease Relevance 0.31 Pain Relevance 0.14
In addition, expression of ADAR1 and ADAR2 does not correspond with editing frequencies of specific target sites in the 5-HT2CR mRNA.
Gene_expression (expression) of ADAR1
5) Confidence 0.61 Published 2009 Journal Mol Brain Section Body Doc Link PMC2694175 Disease Relevance 0 Pain Relevance 0
Overexpression of ADAR1 is shown to inhibit the editing activity of ADAR2 in pediatric astrocytoma, and ADAR1 could co-immunoprecipitate with ADAR2, suggesting a possible mechanism of inhibition via sequestering ADAR2 by ADAR1 in a heterodimer formation [37].
Gene_expression (Overexpression) of ADAR1 associated with anaplastic astrocytoma
6) Confidence 0.61 Published 2009 Journal Mol Brain Section Body Doc Link PMC2694175 Disease Relevance 0.17 Pain Relevance 0
A separate study by Hang et al finds that while expression level of ADAR2 mRNA markedly increases, that of ADAR1 mRNA remains constant during development [45].
Gene_expression (expression) of ADAR1
7) Confidence 0.53 Published 2009 Journal Mol Brain Section Body Doc Link PMC2694175 Disease Relevance 0.06 Pain Relevance 0
Cross-talk among ADAR1, ADAR2 and ADAR3
Gene_expression (talk) of ADAR1
8) Confidence 0.53 Published 2009 Journal Mol Brain Section Body Doc Link PMC2694175 Disease Relevance 0.07 Pain Relevance 0
The deletion of ADAR1 in mice is embryonically lethal, and mice die between E11.5 and 12.5, as the mice develop a severe liver defect that involves cells of both the hematopoietic and hepatic lineages.
Gene_expression (deletion) of ADAR1 in liver
9) Confidence 0.53 Published 2009 Journal Mol Brain Section Body Doc Link PMC2694175 Disease Relevance 0.36 Pain Relevance 0.06
Protein chimeras, in which the deaminase domains were exchanged between ADAR1 and ADAR2, retained the substrate specificity of the donor's deaminase domain [28].
Gene_expression (exchanged) of ADAR1
10) Confidence 0.53 Published 2009 Journal Mol Brain Section Body Doc Link PMC2694175 Disease Relevance 0 Pain Relevance 0
Furthermore, TD in C57BL/6J mice also selectively reduced both mRNA and protein levels of ADAR2, but not that of ADAR1 (Figure 4C, 4D and 4F).
Gene_expression (levels) of ADAR1 associated with thiamine deficiency
11) Confidence 0.51 Published 2010 Journal Mol Neurodegener Section Body Doc Link PMC3006372 Disease Relevance 0.90 Pain Relevance 0
Immunoblotting analysis indicated that TD significantly decreased the expression of ADAR2, but not ADAR1 in cortical neurons (Figure 4A and 4B).
Gene_expression (expression) of ADAR1 in neurons associated with thiamine deficiency
12) Confidence 0.51 Published 2010 Journal Mol Neurodegener Section Body Doc Link PMC3006372 Disease Relevance 0.87 Pain Relevance 0
In this review, we would discuss some potential mechanisms and factors that could dynamically regulate this A-to-I modification by ADAR, namely the expression and activity of ADAR family members via self-editing, alternative splicing and cross-talk between these two mechanisms.
Gene_expression (expression) of ADAR in ADAR
13) Confidence 0.47 Published 2009 Journal Mol Brain Section Body Doc Link PMC2694175 Disease Relevance 0.09 Pain Relevance 0.15
ADAR1 and ADAR2 were shown to be ubiquitously expressed, with enzymatic targets identified mainly in the nervous system while ADAR3 expression is restricted to brain and has yet no known targets [3,23].
Gene_expression (expressed) of ADAR1 in brain
14) Confidence 0.47 Published 2009 Journal Mol Brain Section Body Doc Link PMC2694175 Disease Relevance 0 Pain Relevance 0.09
ADAR1 and ADAR2 are widely detected in various tissues, with strong expression in the brain [30,33].
Gene_expression (detected) of ADAR1 in brain
15) Confidence 0.40 Published 2010 Journal Mol Neurodegener Section Body Doc Link PMC3006372 Disease Relevance 0 Pain Relevance 0.19

General Comments

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