INT51869

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Context Info
Confidence 0.52
First Reported 1995
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 24
Total Number 24
Disease Relevance 10.40
Pain Relevance 2.18

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

plasma membrane (Dmd) cytoskeleton (Dmd) nucleus (Dmd)
cytoplasm (Dmd)
Anatomy Link Frequency
muscle 4
muscle fiber 2
skeletal muscle 1
hippocampus 1
glial cells 1
Dmd (Mus musculus)
Pain Link Frequency Relevance Heat
Hippocampus 108 99.96 Very High Very High Very High
member 8 1 99.68 Very High Very High Very High
fibrosis 39 99.46 Very High Very High Very High
Inflammation 7 99.26 Very High Very High Very High
Pain 3 98.80 Very High Very High Very High
potassium channel 6 97.38 Very High Very High Very High
GABAergic 72 95.72 Very High Very High Very High
Pyramidal cell 36 95.64 Very High Very High Very High
Neurotransmitter 200 91.20 High High
depression 18 87.40 High High
Disease Link Frequency Relevance Heat
Cognitive Disorder 108 100.00 Very High Very High Very High
Congenital Anomalies 116 99.90 Very High Very High Very High
Targeted Disruption 164 99.62 Very High Very High Very High
Colorblindness 18 99.60 Very High Very High Very High
Cramps 6 99.56 Very High Very High Very High
Fibrosis 50 99.46 Very High Very High Very High
Myalgia 6 99.34 Very High Very High Very High
INFLAMMATION 12 99.26 Very High Very High Very High
Frailty 38 99.24 Very High Very High Very High
Duchenne Muscular Dystrophy 36 99.08 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Patients with Duchenne and Becker muscular dystrophy suffer from a progressive deterioration in muscle secondary to a defect in the dystrophin gene.
Negative_regulation (defect) of dystrophin gene in muscle associated with duchenne muscular dystrophy
1) Confidence 0.52 Published 2008 Journal Paediatr Anaesth Section Abstract Doc Link 18184239 Disease Relevance 0.66 Pain Relevance 0.07
In the hippocampus, loss of Dp427 in mdx mice does not affect inhibitory postsynaptic currents (IPSCs; Textbox 2 in “Appendix”) evoked in the pyramidal cell layer [145].
Negative_regulation (loss) of Dp427 in Appendix associated with pyramidal cell and hippocampus
2) Confidence 0.52 Published 2009 Journal Mol Neurobiol Section Body Doc Link PMC2840664 Disease Relevance 0.28 Pain Relevance 0.30
Interestingly, muscle degeneration was observed in larvae, when all dystrophin isoform expression levels, or Dp117 specifically, were reduced in muscle by transgenic RNA interference [37].
Negative_regulation (reduced) of dystrophin in muscle associated with targeted disruption
3) Confidence 0.45 Published 2009 Journal Mol Neurobiol Section Body Doc Link PMC2840664 Disease Relevance 0.22 Pain Relevance 0.05
Thus, this color vision defect may be caused by a loss of the dystrophin isoform Dp260 [159, 168].
Negative_regulation (loss) of dystrophin associated with colorblindness
4) Confidence 0.45 Published 2009 Journal Mol Neurobiol Section Body Doc Link PMC2840664 Disease Relevance 0.51 Pain Relevance 0
Mdx mice are deficient in dystrophin and show muscle fiber regeneration.
Negative_regulation (deficient) of dystrophin in muscle fiber
5) Confidence 0.42 Published 2005 Journal J. Neurocytol. Section Abstract Doc Link 16902760 Disease Relevance 0 Pain Relevance 0.12
Conversely, there were no changes in nNOS distribution and expression in normal regenerated fibers, suggesting that the decrease in nNOS expression reported for mdx mice might be attributed to the absence of dystrophin.
Negative_regulation (absence) of dystrophin
6) Confidence 0.42 Published 2001 Journal Muscle Nerve Section Abstract Doc Link 11353428 Disease Relevance 0 Pain Relevance 0.14
This suggests that changes in AChRs distribution seen in mdx mice were probably a consequence of muscle fiber degeneration and regeneration, rather than a symptom of dystrophin deficiency.
Negative_regulation (deficiency) of dystrophin in muscle fiber
7) Confidence 0.42 Published 2001 Journal Muscle Nerve Section Abstract Doc Link 11353428 Disease Relevance 0 Pain Relevance 0.15
In the present study, we demonstrate that muscular dystrophy is ameliorated in two animal models, dystrophin-deficient mdx mice and delta-sarcoglycan-deficient BIO14.6 hamsters by dominant-negative inhibition of the transient receptor potential cation channel, TRPV2, a principal candidate for Ca(2+)-entry pathways.
Negative_regulation (inhibition) of dystrophin associated with member 8 and frailty
8) Confidence 0.41 Published 2009 Journal Hum. Mol. Genet. Section Abstract Doc Link 19050039 Disease Relevance 0.86 Pain Relevance 0.13
Similar increases associated with dystrophin deficiency were found in EDL and SOL muscles (unpublished data).
Negative_regulation (deficiency) of dystrophin in muscles
9) Confidence 0.39 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2483333 Disease Relevance 0 Pain Relevance 0.24
Additionally, in good agreement with the results obtained by Western blot analysis, we observed a decrease in Nav1.4 channel density in mdx5cv as compared with control fibers (Fig. 6 C).
Negative_regulation (decrease) of mdx5cv
10) Confidence 0.39 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2483333 Disease Relevance 0 Pain Relevance 0
In addition, it has become apparent that results obtained from tests employing the mdx mouse (which only lacks full-length dystrophin isoform Dp427) likely differ from those using the mdx3cv mouse (which lacks all dystrophin isoforms).
Negative_regulation (lacks) of Dp427
11) Confidence 0.38 Published 2009 Journal Mol Neurobiol Section Body Doc Link PMC2840664 Disease Relevance 0.41 Pain Relevance 0.03
Furthermore, studies are reviewed that indicate that a number of the DGC members (dystrophin, dystrobrevin, syntrophin, and dystroglycan) are present at the postsynaptic side of mammalian inhibitory GABAergic synapses in the hippocampus and in cerebellar Purkinje cells [135], where they are required for synapse function and plasticity.
Negative_regulation (number) of dystrophin in synapses associated with gabaergic and hippocampus
12) Confidence 0.38 Published 2009 Journal Mol Neurobiol Section Body Doc Link PMC2840664 Disease Relevance 0.47 Pain Relevance 0.16
The above-mentioned studies, while showing different electrical responses to dystrophin deficiency in the cerebellum versus the hippocampus, suggest that the alteration of inhibitory synaptic transmission may contribute to memory deficits evident in mdx mice.
Negative_regulation (deficiency) of dystrophin in hippocampus associated with hippocampus
13) Confidence 0.38 Published 2009 Journal Mol Neurobiol Section Body Doc Link PMC2840664 Disease Relevance 0.25 Pain Relevance 0.20
Although mdx mice, lacking Dp427, display normal ERG [154], mdxCV3 mice, lacking all dystrophin isoforms, show a decreased b-wave response [165].
Negative_regulation (lacking) of Dp427
14) Confidence 0.38 Published 2009 Journal Mol Neurobiol Section Body Doc Link PMC2840664 Disease Relevance 0.51 Pain Relevance 0
We and others (Ribaux et al., 2001) obtained similar results with EDL muscle where Nav1.4 expression was decreased by 40% in mdx5cv compared with control muscle (unpublished data).
Negative_regulation (decreased) of mdx5cv in muscle
15) Confidence 0.34 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2483333 Disease Relevance 0 Pain Relevance 0.18
In addition, it has become apparent that results obtained from tests employing the mdx mouse (which only lacks full-length dystrophin isoform Dp427) likely differ from those using the mdx3cv mouse (which lacks all dystrophin isoforms).
Negative_regulation (lacks) of dystrophin
16) Confidence 0.33 Published 2009 Journal Mol Neurobiol Section Body Doc Link PMC2840664 Disease Relevance 0.41 Pain Relevance 0.03
Recently, Vaillend and colleagues addressed memory impairment in mdx mice using spatially and nonspatially defined tasks that can be rapidly learned [130].
Negative_regulation (impairment) of mdx associated with cognitive disorder
17) Confidence 0.33 Published 2009 Journal Mol Neurobiol Section Body Doc Link PMC2840664 Disease Relevance 0.44 Pain Relevance 0
Wagner et al. crossed mdx animals with myostatin knockout animals and did not observe any change in heart size or functional parameters at 24 months of age in mdx/Mstat KO animals [48].
Negative_regulation (crossed) of mdx in heart associated with targeted disruption
18) Confidence 0.24 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2820101 Disease Relevance 0.66 Pain Relevance 0
/Smad signaling pathway in myostatin knockout mice or long term inhibition in mdx mice results in reduced specific tension of the EDL that is of questionable therapeutic utility [41].
Negative_regulation (inhibition) of mdx associated with targeted disruption
19) Confidence 0.24 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2820101 Disease Relevance 0.43 Pain Relevance 0
When the expression of nNOS is restored then it has been reported that the inflammation, fibrosis and ECG abnormalities are prevented in the mdx mouse [52].
Negative_regulation (prevented) of mdx associated with fibrosis, inflammation and congenital anomalies
20) Confidence 0.21 Published 2010 Journal The Open Cardiovascular Medicine Journal Section Body Doc Link PMC3024556 Disease Relevance 1.10 Pain Relevance 0.16

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