INT255135

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Context Info
Confidence 0.56
First Reported 2008
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 18
Total Number 24
Disease Relevance 5.84
Pain Relevance 0.43

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

mRNA binding (Celf1) mRNA processing (Celf1) RNA binding (Celf1)
nucleus (Celf1) cytoplasm (Celf1)
Anatomy Link Frequency
myoblasts 4
skeletal muscles 4
muscle 3
heart 3
cardiomyocytes 2
Celf1 (Mus musculus)
Pain Link Frequency Relevance Heat
anesthesia 26 95.96 Very High Very High Very High
GABAergic 20 94.32 High High
Kinase C 6 91.80 High High
Inflammation 7 80.28 Quite High
cytokine 14 59.80 Quite High
tolerance 39 5.00 Very Low Very Low Very Low
imagery 20 5.00 Very Low Very Low Very Low
gABA 18 5.00 Very Low Very Low Very Low
Central nervous system 14 5.00 Very Low Very Low Very Low
fibrosis 12 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 413 100.00 Very High Very High Very High
Congenital Anomalies 185 99.20 Very High Very High Very High
Death 24 95.56 Very High Very High Very High
Arrhythmias 2 Under Development 113 95.28 Very High Very High Very High
Cv General 2 Under Development 48 94.56 High High
Disease 188 94.00 High High
Insulin Resistance 21 91.12 High High
Frailty 136 90.20 High High
Toxicity 238 89.64 High High
Myotonia 98 86.40 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Molecular analysis of the “inducible” transgenic mice with overt DM1 phenotype showed that these mice have increased levels of CUGBP1 (CUG-binding protein 1) [34].
Positive_regulation (increased) of Gene_expression (levels) of CUG-binding protein 1 associated with targeted disruption
1) Confidence 0.56 Published 2010 Journal Current Genomics Section Body Doc Link PMC2874224 Disease Relevance 0.50 Pain Relevance 0
However, transgenic mice overexpressing CUGBP1 developed splicing abnormalities suggesting that misregulation of splicing of CUGBP1 targets in vivo is independent of MBNL1 [68].
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of CUGBP1 associated with targeted disruption and congenital anomalies
2) Confidence 0.56 Published 2010 Journal Current Genomics Section Body Doc Link PMC2874224 Disease Relevance 0.29 Pain Relevance 0
The elevation of CUGBP1 has been also reported for DM2 patients [52]; however, there are contradictory results for expression of CUGBP1 in DM2.
Positive_regulation (results) of Gene_expression (expression) of CUGBP1
3) Confidence 0.56 Published 2010 Journal Current Genomics Section Body Doc Link PMC2874224 Disease Relevance 0.22 Pain Relevance 0
Early elevation of CUGBP1 in transgenic mice expressing CUG repeats shows that the increase of CUGBP1 is not a consequence of different abnormalities in DM1 but rather a direct result of expression of the mutant CUG repeats [64].
Positive_regulation (elevation) of Gene_expression (expressing) of CUGBP1 associated with targeted disruption and congenital anomalies
4) Confidence 0.40 Published 2010 Journal Current Genomics Section Body Doc Link PMC2874224 Disease Relevance 0.29 Pain Relevance 0
Molecular analysis of the “inducible” transgenic mice with overt DM1 phenotype showed that these mice have increased levels of CUGBP1 (CUG-binding protein 1) [34].
Positive_regulation (increased) of Gene_expression (levels) of CUGBP1 associated with targeted disruption
5) Confidence 0.40 Published 2010 Journal Current Genomics Section Body Doc Link PMC2874224 Disease Relevance 0.50 Pain Relevance 0
Given these additional activities of CUGBP1, it is not surprising that lower or high levels of expression of CUGBP1 have a toxic effect on normal development [73,89].
Positive_regulation (levels) of Gene_expression (expression) of CUGBP1
6) Confidence 0.37 Published 2010 Journal Current Genomics Section Body Doc Link PMC2874224 Disease Relevance 0.55 Pain Relevance 0.07
Expression of pure RNA CCUG repeats in normal cells also increased levels of CUGBP1 [52].
Positive_regulation (increased) of Gene_expression (levels) of CUGBP1
7) Confidence 0.33 Published 2010 Journal Current Genomics Section Body Doc Link PMC2874224 Disease Relevance 0.13 Pain Relevance 0
We show that overexpression of CUGBP1 in human SK-N-SH cells, or depletion of MBNL1, result in an upregulation of GABT4 that mimics the in vivo changes in steady state levels caused by CUGexp transcripts.
Positive_regulation (overexpression) of Gene_expression (overexpression) of CUGBP1 in SK-N-SH
8) Confidence 0.32 Published 2009 Journal PLoS Genetics Section Body Doc Link PMC2719092 Disease Relevance 0.08 Pain Relevance 0.08
Transgenic mice that overexpress CUG-BP1 in muscle and heart reproduce missplicing alterations typical of DM1, which has confirmed the involvement of this protein in the pathogenesis of the disease as well as the antagonism between MBNL1 and CUG-BP1 in alternative splicing regulation ([70] and below).
Positive_regulation (overexpress) of Gene_expression (overexpress) of CUG-BP1 in muscle associated with targeted disruption and disease
9) Confidence 0.29 Published 2008 Journal Current Genomics Section Body Doc Link PMC2694559 Disease Relevance 0.44 Pain Relevance 0.05
Cells overexpressing CUGBP1 (p<0.0001) or SCA8 exon A CTGexp minigenes show increases in GABT4 RNA (p?
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of CUGBP1
10) Confidence 0.23 Published 2009 Journal PLoS Genetics Section Body Doc Link PMC2719092 Disease Relevance 0 Pain Relevance 0
Although surprising, the authors explained the DM1 phenotype by the unbalance between CUG-BP1 (upregulated) and Mbnl1 (unchanged) antagonistic activities as alternative splicing regulators resulting in missplicing of characteristic transcripts such as ClC-1 and cTNT [72].
Positive_regulation (upregulated) of Gene_expression (phenotype) of CUG-BP1
11) Confidence 0.21 Published 2008 Journal Current Genomics Section Body Doc Link PMC2694559 Disease Relevance 0.41 Pain Relevance 0
Transgenic mice that overexpress CUG-BP1 in muscle and heart reproduce missplicing alterations typical of DM1, which has confirmed the involvement of this protein in the pathogenesis of the disease as well as the antagonism between MBNL1 and CUG-BP1 in alternative splicing regulation ([70] and below).
Positive_regulation (overexpress) of in heart Gene_expression (overexpress) of CUG-BP1 in muscle associated with targeted disruption and disease
12) Confidence 0.10 Published 2008 Journal Current Genomics Section Body Doc Link PMC2694559 Disease Relevance 0.44 Pain Relevance 0.05
Cug-bp1 levels are elevated in ?
Positive_regulation (elevated) of Gene_expression (levels) of Cug-bp1
13) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2597774 Disease Relevance 0 Pain Relevance 0
Thus these results demonstrate that although increased steady state levels of CUG-BP1 is sufficient to produce features of DM1, elevated CUG-BP1 levels may not be required for DM1 pathology to manifest, as reduction of CUG-BP1 levels does not correct the splice defects in DM1 myoblasts.
Neg (not) Positive_regulation (required) of Gene_expression (levels) of CUG-BP1 in myoblasts
14) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2597774 Disease Relevance 0.33 Pain Relevance 0
2.5 fold increase in Cug-bp1 levels in ?
Positive_regulation (increase) of Gene_expression (levels) of Cug-bp1
15) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2597774 Disease Relevance 0 Pain Relevance 0
-actin gene does not result in elevated Cug-bp1 levels in mouse skeletal muscles [35].
Neg (not) Positive_regulation (result) of Gene_expression (levels) of Cug-bp1 in skeletal muscles
16) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2597774 Disease Relevance 0 Pain Relevance 0
Significantly, steady state Cug-bp1 levels are elevated ?
Positive_regulation (elevated) of Gene_expression (levels) of Cug-bp1
17) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2597774 Disease Relevance 0 Pain Relevance 0
Cug-bp1 levels were elevated ?
Positive_regulation (elevated) of Gene_expression (levels) of Cug-bp1
18) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2597774 Disease Relevance 0 Pain Relevance 0
Thus these results demonstrate that although increased steady state levels of CUG-BP1 is sufficient to produce features of DM1, elevated CUG-BP1 levels may not be required for DM1 pathology to manifest, as reduction of CUG-BP1 levels does not correct the splice defects in DM1 myoblasts.
Positive_regulation (elevated) of Gene_expression (levels) of CUG-BP1 in myoblasts
19) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2597774 Disease Relevance 0.33 Pain Relevance 0
In these experiments Cug-bp1 was found to localize primarily in the cytoplasm in both ?
Positive_regulation (experiments) of Gene_expression (found) of Cug-bp1
20) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2597774 Disease Relevance 0 Pain Relevance 0

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