INT211095

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Context Info
Confidence 0.57
First Reported 2007
Last Reported 2009
Negated 0
Speculated 1
Reported most in Body
Documents 14
Total Number 17
Disease Relevance 7.18
Pain Relevance 1.07

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

nucleoplasm (Dag1) extracellular space (Dag1) extracellular region (Dag1)
plasma membrane (Dag1) cytoskeleton (Dag1) nucleus (Dag1)
Anatomy Link Frequency
retinas 3
glial cells 2
neurons 1
brain 1
Dag1 (Mus musculus)
Pain Link Frequency Relevance Heat
potassium channel 78 99.16 Very High Very High Very High
Glutamate receptor 18 98.40 Very High Very High Very High
ischemia 29 93.44 High High
Inflammatory mediators 65 84.16 Quite High
Inflammation 45 83.28 Quite High
Hippocampus 36 83.20 Quite High
Neurotransmitter 92 67.84 Quite High
antagonist 3 63.76 Quite High
depression 6 59.68 Quite High
long-term potentiation 3 54.44 Quite High
Disease Link Frequency Relevance Heat
Targeted Disruption 46 99.76 Very High Very High Very High
Retina Disease 325 99.20 Very High Very High Very High
Blister 8 98.72 Very High Very High Very High
Gliosis 94 98.48 Very High Very High Very High
Bullous Skin Disease 75 97.56 Very High Very High Very High
Pressure And Volume Under Development 261 96.88 Very High Very High Very High
Stress 42 95.56 Very High Very High Very High
Disease 71 94.52 High High
Cv Unclassified Under Development 29 93.44 High High
Death 14 91.48 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These alterations are associated with a strong decrease of Dp71, a cytoskeleton protein responsible for the localization and the clustering of Kir4.1 and AQP4.
Negative_regulation (decrease) of Dp71
1) Confidence 0.57 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2754330 Disease Relevance 0.31 Pain Relevance 0.08
By using Western blotting and subsequent semiquantification of band densities of Dp71, we observed a dramatic reduction of Dp71 protein in detached retinas (Fig. 3A), by about 50% (Fig. 3B).
Negative_regulation (reduction) of Dp71 in retinas
2) Confidence 0.57 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2754330 Disease Relevance 0.29 Pain Relevance 0
Our present results confirm that functional expression of Dp71 is necessary for the highly asymmetric expression of the inwardly rectifying potassium channel Kir4.1 in Müller cells, and suggest that Dp71 downregulation is one step upstream of the Kir4.1 and AQP4 channel alterations in the signaling cascade of reactive gliosis.
Negative_regulation (downregulation) of Dp71 associated with potassium channel and gliosis
3) Confidence 0.57 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2754330 Disease Relevance 0.38 Pain Relevance 0.05
Furthermore, we show that the early, acute downregulation of Dp71 in normal animals may be an important, decisive step in the development of reactive gliosis, upstream of the physiological alterations.
Negative_regulation (downregulation) of Dp71 associated with gliosis
4) Confidence 0.50 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2754330 Disease Relevance 0.23 Pain Relevance 0
Partial (in detached retinas) or total depletion of Dp71 in Müller cells (in Dp71-null mice) impairs the capability of volume regulation of Müller cells under osmotic stress.
Negative_regulation (depletion) of Dp71 in retinas associated with stress
5) Confidence 0.50 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2754330 Disease Relevance 0.35 Pain Relevance 0.09
This finding shows that partial or total depletion of Dp71 in Müller cells are associated with alterations in transmembraneous water transport.
Spec (partial) Negative_regulation (depletion) of Dp71
6) Confidence 0.50 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2754330 Disease Relevance 0.73 Pain Relevance 0.12
Using an experimental mouse model of retinal detachment, we (i) confirm morpho-functional alterations in reactive Müller glial cells including a mislocation of Kir4.1 potassium channels and a downregulation of AQP4 water channels, accompanied by disturbed volume regulation of the cells; (ii) show a fast and strong decrease of the dystrophin protein, Dp71; and finally (iii) demonstrate an impaired BRB function as evidenced by increased retinal vascular permeability.
Negative_regulation (decrease) of Dp71 in glial cells associated with potassium channel and retina disease
7) Confidence 0.42 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2754330 Disease Relevance 0.15 Pain Relevance 0.05
Thus suggesting that Dp71 depletion did not induce reactive Müller cells gliosis.


Negative_regulation (depletion) of Dp71 associated with gliosis
8) Confidence 0.42 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2754330 Disease Relevance 0.51 Pain Relevance 0.04
In conclusion we show here that depletion of Dp71, a cytoskeleton protein associated to the membrane, leads to physiological alterations in Müller cells similar to those observed in injured or diseased retinas; this involves a mislocation of potassium and water channels (Kir4.1 and AQP4) and a consequent dysregulation of water transport through Müller cells.
Negative_regulation (depletion) of Dp71 in retinas
9) Confidence 0.42 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2754330 Disease Relevance 0.06 Pain Relevance 0
This idea is further supported if the consequences of Dp71 deficiency are studied one step downstream of the channel alterations, by assessing the swelling properties of Müller cells.
Negative_regulation (deficiency) of Dp71 associated with pressure and volume under development
10) Confidence 0.42 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2754330 Disease Relevance 0.53 Pain Relevance 0.07
Genetic inactivation of Dp71 (in Dp71-null mice) alters Kir4.1 and AQP4 distribution in Müller glial cells and this mislocation increases the vulnerability of retinal nerve cells to transient ischemia which is associated with neuronal cells death [14], [15].
Negative_regulation (inactivation) of Dp71 in glial cells associated with ischemia and death
11) Confidence 0.42 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2754330 Disease Relevance 0.49 Pain Relevance 0.14
Summarizing these results, both gene and protein expression of Dp71 are strongly reduced after experimental retinal detachment in C57BL/6 mice.
Negative_regulation (reduced) of Dp71 associated with retina disease
12) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2754330 Disease Relevance 0.30 Pain Relevance 0
First, the fluid transport through Müller cell membrane is impaired (Fig. 5) and second, we show here for the first time that Dp71 depletion is accompanied by a significantly increased retinal vascular permeability (Fig. 6).
Negative_regulation (depletion) of Dp71
13) Confidence 0.36 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2754330 Disease Relevance 0.36 Pain Relevance 0.06
Finally, the effects of the loss of the Dp71 isoform on mouse brain function employing electrophysiology and behavioral studies were recently reported [152].
Negative_regulation (loss) of Dp71 isoform in brain
14) Confidence 0.31 Published 2009 Journal Mol Neurobiol Section Body Doc Link PMC2840664 Disease Relevance 0.31 Pain Relevance 0.21
Mice that only lack Dp71 [166] have normal ERGs with no significant changes of the b-wave amplitude and kinetics [167].
Negative_regulation (lack) of Dp71
15) Confidence 0.27 Published 2009 Journal Mol Neurobiol Section Body Doc Link PMC2840664 Disease Relevance 0.62 Pain Relevance 0
Interestingly, glutamatergic transmission is enhanced and synaptic plasticity reduced in Dp71-deficient CA1 hippocampal neurons.
Negative_regulation (reduced) of Dp71 in neurons
16) Confidence 0.27 Published 2009 Journal Mol Neurobiol Section Body Doc Link PMC2840664 Disease Relevance 0.30 Pain Relevance 0.17
Inactivation of DG III in a knock-out mouse model results in lesions similar to those in patients with PV (Koch et al 1997).
Negative_regulation (Inactivation) of DG III associated with targeted disruption and bullous skin disease
17) Confidence 0.02 Published 2007 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC1936286 Disease Relevance 1.26 Pain Relevance 0

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