INT158463

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Context Info
Confidence 0.31
First Reported 2007
Last Reported 2010
Negated 1
Speculated 1
Reported most in Body
Documents 7
Total Number 9
Disease Relevance 4.87
Pain Relevance 0.40

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

nucleus (Hmbs) cytoplasm (Hmbs)
Anatomy Link Frequency
neuronal 1
immune system 1
Hmbs (Mus musculus)
Pain Link Frequency Relevance Heat
isoflurane 5 89.12 High High
fibrosis 2 80.44 Quite High
Glutamate receptor 3 71.56 Quite High
anesthesia 2 66.04 Quite High
Inflammation 28 61.24 Quite High
Dopamine 33 56.32 Quite High
Glutamate 6 37.84 Quite Low
midbrain 12 5.00 Very Low Very Low Very Low
Central nervous system 9 5.00 Very Low Very Low Very Low
Spinal cord 8 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Porphyria 3 100.00 Very High Very High Very High
Disease 311 98.48 Very High Very High Very High
Targeted Disruption 46 96.92 Very High Very High Very High
Diabetes Mellitus 73 95.96 Very High Very High Very High
Frailty 38 93.88 High High
Stress 54 92.32 High High
Parkinson's Disease 147 89.44 High High
Diabetic Retinopathy 7 88.48 High High
Congenital Anomalies 1 87.28 High High
Chronic Renal Failure 56 87.12 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Covalent linkage of ubiquitin regulates the function and, ultimately, the degradation of many proteins by the ubiquitin-proteasome system (UPS).
Regulation (regulates) of UPS
1) Confidence 0.31 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2690827 Disease Relevance 0.22 Pain Relevance 0
No alterations were found in either PBG-D or HO activities.
Neg (No) Regulation (alterations) of PBG-D associated with porphyria
2) Confidence 0.22 Published 2009 Journal Cell. Mol. Biol. (Noisy-le-grand) Section Abstract Doc Link 19268000 Disease Relevance 0.77 Pain Relevance 0.26
Ultimately, such findings with our transgenic mouse model could be utilized to identify key therapeutic timepoints in the disease process, and to develop and screen therapeutic agents for the potential to modulate UPS function at these timepoints.


Regulation (modulate) of UPS associated with targeted disruption and disease
3) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2690827 Disease Relevance 0.61 Pain Relevance 0
Over the past two decades, progress in understanding the action and regulation of the UPS has been at the center of attempts to understand the control of protein turnover.
Regulation (regulation) of UPS
4) Confidence 0.11 Published 2007 Journal Pediatr Nephrol Section Body Doc Link PMC2259254 Disease Relevance 0.59 Pain Relevance 0.03
Influencing the function of the immune system The UPS is responsible for creating antigens from the degradation of foreign proteins (e.g. viral particles).
Regulation (Influencing) of UPS in immune system
5) Confidence 0.08 Published 2007 Journal Pediatr Nephrol Section Body Doc Link PMC2259254 Disease Relevance 0.26 Pain Relevance 0.04
This is another point of intersection between mitochondria and UPS functioning, since mitochondria, producing excessive ROS, may adversely affect UPS activity.
Spec (may) Regulation (affect) of UPS
6) Confidence 0.08 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2890153 Disease Relevance 0.61 Pain Relevance 0.06
Mutations in parkin and uchl1 genes are related with alterations in the UPS pathway.
Regulation (alterations) of UPS
7) Confidence 0.08 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2890153 Disease Relevance 0.52 Pain Relevance 0
Our results show that in the absence of a functional mitochondria, due to mitochondrial DNA knockdown, the UPS is down-regulated.
Regulation (regulated) of UPS
8) Confidence 0.08 Published 2010 Journal Frontiers in Aging Neuroscience Section Body Doc Link PMC2890153 Disease Relevance 0.46 Pain Relevance 0
The protein, but not mRNA, reduction of synaptophysin in neuronal cells was shown to depend on the UPS, which was enhanced via AT1R signaling (Fig. 4).
Regulation (depend) of UPS in neuronal
9) Confidence 0.04 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.82 Pain Relevance 0

General Comments

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