INT120175

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Context Info
Confidence 0.57
First Reported 2004
Last Reported 2008
Negated 1
Speculated 1
Reported most in Body
Documents 10
Total Number 11
Disease Relevance 2.57
Pain Relevance 0.92

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

cytosol (HK1) mitochondrion (HK1) small molecule metabolic process (HK1)
nucleolus (HK1) nucleus (HK1) carbohydrate metabolic process (HK1)
Anatomy Link Frequency
muscle 2
internal 1
central nervous system 1
HK1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Central nervous system 169 98.60 Very High Very High Very High
Pain 3 96.08 Very High Very High Very High
Glutamate 8 89.04 High High
Inflammatory mediators 1 85.08 High High
cva 193 83.52 Quite High
anesthesia 33 69.00 Quite High
Catecholamine 3 57.52 Quite High
ketamine 16 48.16 Quite Low
cerebral cortex 16 25.28 Quite Low
Paracetamol 2 24.64 Low Low
Disease Link Frequency Relevance Heat
Glycogen Storage Disease 4 99.24 Very High Very High Very High
Disease 24 98.72 Very High Very High Very High
Diabetes Mellitus 26 97.52 Very High Very High Very High
Parkinson's Disease 25 96.40 Very High Very High Very High
Pain 3 95.92 Very High Very High Very High
Stress 11 94.92 High High
Hyperglycemia 25 93.76 High High
Death 6 93.44 High High
INFLAMMATION 3 84.68 Quite High
Hypoxia 1 84.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Peroxy-nitrite, superoxide, and other reactive oxygen species lead to inhibition of the glycolytic enzyme glyceraldhyde phosphate dehydrogenase and mitochondrial complexes I and IV, the basis of mitochondrial dysfunction likely to induce end-organ failure and cellular death [114].
Negative_regulation (inhibition) of glycolytic enzyme associated with parkinson's disease and death
1) Confidence 0.57 Published 2008 Journal Crit Care Section Body Doc Link PMC2646334 Disease Relevance 1.51 Pain Relevance 0.27
As shown in Figure 2C, the LD domain sharply reversed the inhibitory effect of Cox11 on HKI activity in a concentration-dependent manner, but under saturating (and stochiometric) amounts of LD, the velocity of the reaction did not reach that observed for HKI activity in the absence of Cox11 (Figure 2A), suggesting the LD by itself may also have an effect on HKI activity.
Negative_regulation (reversed) of HKI
2) Confidence 0.23 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0 Pain Relevance 0
For example, the combination of the CLD of RanBP2 with several subunits of the 19S cap of the proteasome [14], and of its neighboring internal repeat, W1W2/IR with the E3-ubiquitin ligase, parkin [20], and the E2 SUMO-1-conjugating protein, Ubc9 [15] may contribute to the down-regulation of HKI by 26S proteasome-mediated proteolysis and modulation of the molecular and subcellular partitioning of these partners.
Negative_regulation (regulation) of HKI in internal
3) Confidence 0.17 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0 Pain Relevance 0.03
The sub-stochiometry effect of the LD of RanBP2 over the inhibition of HKI by Cox11 supports that a LD-dependent chaperonin-like mechanism underlies the suppression of Cox11-dependent inhibition of HKI by RanBP2, and that RanBP2 acts as a molecular “buffer” over HK1 and Cox11 activities.
Negative_regulation (inhibition) of HKI
4) Confidence 0.17 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0 Pain Relevance 0
The data herein show tissues with a decrease of RanBP2 and HKI levels mirror a reduction in the ATP levels.
Negative_regulation (decrease) of HKI
5) Confidence 0.17 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0.22 Pain Relevance 0.19
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).
Neg (not) Negative_regulation (reduced) of HKI
6) Confidence 0.15 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0 Pain Relevance 0
Moreover, partial loss-of-function of RanBP2 in a mouse model induces deficits in growth rates and breakdown of glucose, promotes the down-regulation of HKI and ATP levels selectively in the central nervous system, and impairs visual function.
Negative_regulation (regulation) of HKI in central nervous system associated with central nervous system
7) Confidence 0.15 Published 2006 Journal PLoS Genetics Section Abstract Doc Link PMC1626108 Disease Relevance 0.05 Pain Relevance 0.05
Cox11 behaves as a partial noncompetitive inhibitor of HKI by affecting the Vmax of HKI for glucose (Figure 2B).
Spec (partial) Negative_regulation (inhibitor) of HKI
8) Confidence 0.15 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0 Pain Relevance 0
This is reflected by a reduction of the Vmax of HKI without significantly affecting the Km of the active site of HKI toward glucose (Figure 2A and 2B).
Negative_regulation (reduction) of HKI
9) Confidence 0.14 Published 2006 Journal PLoS Genetics Section Body Doc Link PMC1626108 Disease Relevance 0 Pain Relevance 0.19
BACKGROUND: McArdle's disease (Glycogen Storage Disease type V) is caused by the absence of the glycolytic enzyme, muscle phosphorylase.
Negative_regulation (absence) of glycolytic enzyme in muscle associated with glycogen storage disease and disease
10) Confidence 0.11 Published 2004 Journal Cochrane Database Syst Rev Section Abstract Doc Link 15266486 Disease Relevance 0.44 Pain Relevance 0.10
BACKGROUND: McArdle disease (Glycogen Storage Disease type V) is caused by the absence of the glycolytic enzyme, muscle phosphorylase.
Negative_regulation (absence) of glycolytic enzyme in muscle associated with glycogen storage disease and disease
11) Confidence 0.04 Published 2008 Journal Cochrane Database Syst Rev Section Abstract Doc Link 18425888 Disease Relevance 0.35 Pain Relevance 0.10

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