INT84572

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Context Info
Confidence 0.07
First Reported 1999
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 67
Total Number 67
Disease Relevance 37.61
Pain Relevance 5.86

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

nucleolus (Zmat3)
Anatomy Link Frequency
liver 7
muscles 7
pyramidal neurons 3
P19 1
plasma 1
Zmat3 (Mus musculus)
Pain Link Frequency Relevance Heat
Pyramidal cell 82 99.88 Very High Very High Very High
Inflammation 451 99.68 Very High Very High Very High
ischemia 56 98.44 Very High Very High Very High
Morphine 6 97.88 Very High Very High Very High
Hippocampus 116 97.68 Very High Very High Very High
depression 171 97.56 Very High Very High Very High
Neuropathic pain 1 96.28 Very High Very High Very High
Action potential 14 96.24 Very High Very High Very High
melanocortin 1 receptor 77 94.60 High High
Pain 39 92.72 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 1656 100.00 Very High Very High Very High
Injury 888 100.00 Very High Very High Very High
Sprains And Strains 183 100.00 Very High Very High Very High
Urological Neuroanatomy 58 99.98 Very High Very High Very High
Prostate Cancer 21 99.76 Very High Very High Very High
Disease 425 99.72 Very High Very High Very High
INFLAMMATION 591 99.68 Very High Very High Very High
Apoptosis 92 99.62 Very High Very High Very High
Death 228 99.32 Very High Very High Very High
Diabetes Mellitus 120 98.70 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Mutations in the VCP gene have been shown to trigger cell death with apoptotic features, whereas expression of wild-type protein has been suggested to have an anti-apoptotic effect [34], [35], [36].
Gene_expression (expression) of wild-type protein associated with apoptosis and death
1) Confidence 0.07 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2950155 Disease Relevance 0.92 Pain Relevance 0
By extension, this supports the conclusion that the properties of transplanted muscles have no effect on innervation status in either wild-type or B6.SOD1 transgenic mice.


Gene_expression (transgenic mice) of wild-type in muscles associated with targeted disruption
2) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.10 Pain Relevance 0
Hindlimb muscles were transplanted between wild-type and SOD1G93A transgenic mice and the innervation status of neuromuscular junctions (NMJs) was examined after 2 months.
Gene_expression (transplanted) of wild-type in NMJs associated with targeted disruption
3) Confidence 0.05 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2842435 Disease Relevance 0.36 Pain Relevance 0
The observation that transplanted wild-type muscles do not inhibit the occurrence of muscle denervation in B6.SOD1 mice provides increased confidence that expression of the G93A SOD1 mutation in muscle is not necessary for the appearance of muscle denervation or the motor neuron disease phenotype.
Gene_expression (muscles) of wild-type in muscles associated with motor neuron diseases
4) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.33 Pain Relevance 0
This is consistent with the results of a previous study in which muscles continued expressing a transgene following transplantation into wild-type hosts [23].
Gene_expression (expressing) of wild-type in muscles
5) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.15 Pain Relevance 0
The results of an earlier study in which muscles were transplanted between SOD1G93A and wild-type mice suggested that muscle may exert a toxic influence in SOD1G93A mice [14].
Gene_expression (transplanted) of wild-type in muscle
6) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.49 Pain Relevance 0.04
The results also show that NMJ innervation status in wild-type muscles transplanted into B6.SOD1 mice is equivalent to the contralateral control side.
Gene_expression (muscles) of wild-type in muscles
7) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.43 Pain Relevance 0
Another explanation for the nearly complete innervation of B6.SOD1 MG transplants by wild-type motor neurons is that the regenerated fibers in transplants do not express the mutant SOD1 protein.
Gene_expression (motor neurons) of wild-type in motor neurons
8) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.05 Pain Relevance 0
However, when motor neuron-Schwann cell combinations are present in wild-type muscles transplanted into B6.SOD1 mice and both cell types likely express the SOD1G93A mutation, nerve terminal degeneration proceeds in a manner indistinguishable from the contralateral, control side.
Gene_expression (muscles) of wild-type in muscles
9) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.09 Pain Relevance 0
Selective regeneration of muscle fibers in transplanted muscles provides another possible explanation for the success of wild-type innervation of B6.SOD1 muscles.
Gene_expression (innervation) of wild-type in muscles
10) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.33 Pain Relevance 0
A loss of function phenotype would be hidden by a transgenic approach for two reasons: 1) the two endogenous wild type alleles can support synthesis of sufficient amounts of functional wild type protein: 2) the over-expression of a partial loss of function mutant protein may augment rather then decrease that function, as may happen in the disease.
Gene_expression (synthesis) of wild type protein associated with targeted disruption and disease
11) Confidence 0.03 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2774945 Disease Relevance 1.13 Pain Relevance 0
This suggested that although the p21+/- mice retained a wild-type allele, this allele was functionally modulated by hypermethylation, and that the inability of sulindac to inhibit tumor formation in Apc+/-, p21+/- mice is likely due to the inability to induce expression of the wild-type, but differentially methylated, p21 allele.
Gene_expression (expression) of wild-type associated with cancer
12) Confidence 0.03 Published 2005 Journal Oncogene Section Abstract Doc Link 15688007 Disease Relevance 0.50 Pain Relevance 0.06
Accordingly, we used the PC3N-A6-WT and PC3N-A6-RR prostate cancer cells that express equivalent levels of the wild-type A6 subunit (cleavable to A6p via uPA treatment) and the non-cleavable subunit, respectively (Fig. 1a).
Gene_expression (express) of wild-type A6 subunit associated with prostate cancer
13) Confidence 0.02 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2570216 Disease Relevance 1.12 Pain Relevance 0.35
Overexpression of the wild-type SPT1 subunit lowers desoxysphingolipid levels and rescues the phenotype of HSAN1.
Gene_expression (Overexpression) of wild-type SPT1 subunit
14) Confidence 0.02 Published 2009 Journal J. Neurosci. Section Title Doc Link 19923297 Disease Relevance 0.46 Pain Relevance 0.09
We selected this model (line D PDGFb-SNCA) which overexpresses wild-type human SNCA from the PDGFb promoter, in part, based on the fact that increased expression of wild-type SNCA in humans can cause PD, as demonstrated in families with autosomal dominant PD due to duplication or triplication of the normal (wild-type) SNCA gene [21], [22], [47], [48].
Gene_expression (expression) of wild-type associated with disease
15) Confidence 0.02 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 0.52 Pain Relevance 0
We selected this model (line D PDGFb-SNCA) which overexpresses wild-type human SNCA from the PDGFb promoter, in part, based on the fact that increased expression of wild-type SNCA in humans can cause PD, as demonstrated in families with autosomal dominant PD due to duplication or triplication of the normal (wild-type) SNCA gene [21], [22], [47], [48].
Gene_expression (overexpresses) of wild-type associated with disease
16) Confidence 0.02 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 0.58 Pain Relevance 0
Mice overexpressing wild-type human SNCA from the platelet-derived growth factor beta (PDGFb) promoter (line D PDGFb-SNCA) are reported to develop motor impairments in association with progressive loss of dopaminergic terminals [20].
Gene_expression (overexpressing) of wild-type in platelet
17) Confidence 0.02 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 1.31 Pain Relevance 0.24
Most remarkably, we could not detect any major form of aggregates of protein Tau in pyramidal neurons that expressed either wild-type or mutant protein Tau.
Gene_expression (expressed) of wild-type in pyramidal neurons associated with pyramidal cell
18) Confidence 0.02 Published 2010 Journal International Journal of Alzheimer's Disease Section Body Doc Link PMC2938448 Disease Relevance 0.17 Pain Relevance 0.13
Here, we review data and insights obtained with adeno-associated viral vectors that were engineered to express wild-type or mutant APP or protein Tau in pyramidal neurons of the hippocampus of wild-type mice.
Gene_expression (express) of wild-type in pyramidal neurons associated with pyramidal cell and hippocampus
19) Confidence 0.02 Published 2010 Journal International Journal of Alzheimer's Disease Section Body Doc Link PMC2938448 Disease Relevance 0.86 Pain Relevance 0.10
Similar expression of wild-type human APP695 failed to produce any deposition of amyloid or of the related effects observed with mutant APP.SLA [30].
Gene_expression (expression) of wild-type associated with alzheimer's dementia
20) Confidence 0.02 Published 2010 Journal International Journal of Alzheimer's Disease Section Body Doc Link PMC2938448 Disease Relevance 0.59 Pain Relevance 0.19

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