INT198495

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Context Info
Confidence 0.78
First Reported 2006
Last Reported 2006
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 24
Disease Relevance 3.31
Pain Relevance 3.14

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

isomerase activity (Ranbp2) protein folding (Ranbp2) transport (Ranbp2)
nucleus (Ranbp2) intracellular (Ranbp2)
Anatomy Link Frequency
neuronal 2
fat 2
retina 1
brain 1
hippocampus 1
Ranbp2 (Mus musculus)
Pain Link Frequency Relevance Heat
Central nervous system 504 99.56 Very High Very High Very High
tolerance 144 98.62 Very High Very High Very High
Hippocampus 24 98.32 Very High Very High Very High
addiction 24 98.16 Very High Very High Very High
cerebral cortex 48 75.52 Quite High
Glutamate 24 53.36 Quite High
anesthesia 96 44.76 Quite Low
ketamine 48 23.92 Low Low
imagery 48 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Impaired Glucose Tolerance 96 98.48 Very High Very High Very High
Diabetic Retinopathy 24 96.56 Very High Very High Very High
Diabetes Mellitus 72 95.58 Very High Very High Very High
Metabolic Disorder 24 95.22 Very High Very High Very High
Body Weight 48 85.68 High High
Viral Infection 24 84.80 Quite High
Ganglion Cysts 24 66.84 Quite High
Congenital Anomalies 24 62.88 Quite High
Aging 48 61.36 Quite High
Neurodegenerative Disease 24 60.44 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In light of the prominent expression of RanBP2 and HKI in retinal neurons [1,19], the vital dependence of the neuronal retina (and brain) on glucose as the main substrate source for energy production, and the determinant impact of metabolic disorders, such as diabetes, in retinal function (e.g., diabetic retinopathy) [37], we probed the impact of deficits in RanBP2, HKI, and ATP, on the electrophysiological responses of subclasses (rod and cone) photoreceptor and postreceptor retinal neurons of RanBP2+/?
Gene_expression (expression) of RanBP2 in neurons associated with addiction, metabolic disorder, diabetes mellitus and diabetic retinopathy
1) Confidence 0.78 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.33 Pain Relevance 0.12
Regardless, lower levels of HKI likely contribute to the decreased levels in ATP, slower growth rates, and diminished ability to metabolize glucose of RanBP2+/?
Gene_expression (glucose) of RanBP2
2) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0 Pain Relevance 0
Cox 11 Inhibits HKI Activity and the LD of RanBP2 Reverses the Inhibition of Cox11 over HKI
Gene_expression (over) of RanBP2
3) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0 Pain Relevance 0
Yet, haploinsufficiency of RanBP2 (this work) and Nup96 [58] predominantly produce, instead, CNS-restricted deficits in energy metabolism and alterations in the immune system linked to the down-regulation of interferon-?
Gene_expression (produce) of RanBP2 in immune system associated with central nervous system
4) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.26 Pain Relevance 0.08
This deficit was rescued in RanBP2+/?
Gene_expression (/) of RanBP2
5) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.16 Pain Relevance 0.29
The scotopic (dark-adapted) responses mediated by the rod photoreceptor pathway at low-stimulus intensities and mixed rod and cone pathways at high-stimulus intensities were substantially reduced in RanBP2+/?
Gene_expression (/) of RanBP2 in photoreceptor
6) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.25 Pain Relevance 0.06
Beginning at around 4 mo of age, RanBP2+/?
Gene_expression (/) of RanBP2
7) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.08 Pain Relevance 0.22
In light of the prominent expression of RanBP2 and HKI in retinal neurons [1,19], the vital dependence of the neuronal retina (and brain) on glucose as the main substrate source for energy production, and the determinant impact of metabolic disorders, such as diabetes, in retinal function (e.g., diabetic retinopathy) [37], we probed the impact of deficits in RanBP2, HKI, and ATP, on the electrophysiological responses of subclasses (rod and cone) photoreceptor and postreceptor retinal neurons of RanBP2+/?
Gene_expression (neurons) of RanBP2 in neuronal associated with addiction, metabolic disorder, diabetes mellitus and diabetic retinopathy
8) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.29 Pain Relevance 0.08
mice on a higher fat diet (~10% fat) performed significantly worse in the glucose tolerance test beginning at 6 mo of age (Figure 7A and 7B), thus supporting that the RanBP2+/?
Gene_expression (/) of RanBP2 in fat associated with tolerance and impaired glucose tolerance
9) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.16 Pain Relevance 0.30
This deficit was rescued in RanBP2+/?
Gene_expression (rescued) of RanBP2
10) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.16 Pain Relevance 0.30
In contrast to mice placed on a normal chow diet (~5% fat; unpublished data), RanBP2+/?
Gene_expression (/) of RanBP2 in fat
11) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.17 Pain Relevance 0.29
The partial loss of the RanBP2 chaperone activity in RanBP2+/?
Gene_expression (activity) of RanBP2
12) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0 Pain Relevance 0
The data support that the ultimate pathophysiological outcome in HKI, caused by a reduction in RanBP2 levels and its chaperone activity, is the selective degradation of HKI as reflected by the reduced levels of HKI (and ATP) but not of other mitochondrial and NPC components (Figure 5).
Gene_expression (levels) of RanBP2
13) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0 Pain Relevance 0
To this end, the administration of the gluconeogenic substrate precursor, pyruvate (pyruvate tolerance test), showed that there was no difference in glucose production in RanBP2+/?
Gene_expression (/) of RanBP2 associated with tolerance
14) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.07 Pain Relevance 0.22
In light of the prominent expression of RanBP2 and HKI in retinal neurons [1,19], the vital dependence of the neuronal retina (and brain) on glucose as the main substrate source for energy production, and the determinant impact of metabolic disorders, such as diabetes, in retinal function (e.g., diabetic retinopathy) [37], we probed the impact of deficits in RanBP2, HKI, and ATP, on the electrophysiological responses of subclasses (rod and cone) photoreceptor and postreceptor retinal neurons of RanBP2+/?
Gene_expression (/) of RanBP2 in neuronal associated with addiction, metabolic disorder, diabetes mellitus and diabetic retinopathy
15) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.29 Pain Relevance 0.08
In addition, RanBP2+/?
Gene_expression (/) of RanBP2
16) Confidence 0.67 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.09 Pain Relevance 0.29
Although the levels of RanBP2 were decreased in the retina, brain, and hippocampus of RanBP2+/?
Gene_expression (levels) of RanBP2 in retina associated with hippocampus
17) Confidence 0.60 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.13 Pain Relevance 0.16
To determine the physiological implications of the interaction between RanBP2 and HKI (and other partners), we employed a murine embryonic stem 129Ola cell line with a targeted RanBP2 locus produced by gene-trapping to produce stable inbred (coisogenic) and mixed background lines, respectively (Figure 4A and 4B).
Gene_expression (produced) of RanBP2 in stem
18) Confidence 0.60 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.06 Pain Relevance 0.04
The partial loss of the RanBP2 chaperone activity in RanBP2+/?
Gene_expression (activity) of RanBP2
19) Confidence 0.59 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0 Pain Relevance 0
This is further evidenced by the presence of genetic modifiers in RanBP2+/?
Gene_expression (presence) of RanBP2
20) Confidence 0.59 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.07 Pain Relevance 0.07

General Comments

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