INT134945

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Context Info
Confidence 0.37
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 5
Disease Relevance 3.69
Pain Relevance 0.24

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

small molecule metabolic process (GBA) hydrolase activity, acting on glycosyl bonds (GBA) cell death (GBA)
carbohydrate metabolic process (GBA) lipid metabolic process (GBA)
GBA (Homo sapiens)
Pain Link Frequency Relevance Heat
Pain 11 77.52 Quite High
magnetoencephalography 5 70.24 Quite High
Neuropathic pain 1 46.00 Quite Low
Inflammation 18 45.16 Quite Low
Central nervous system 15 38.52 Quite Low
cytokine 6 5.00 Very Low Very Low Very Low
palliative 3 5.00 Very Low Very Low Very Low
primary somatosensory cortex 3 5.00 Very Low Very Low Very Low
peripheral neuropathy 3 5.00 Very Low Very Low Very Low
Potency 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Parkinson's Disease 24 98.80 Very High Very High Very High
Disease 47 98.60 Very High Very High Very High
Tinnitus 47 94.96 High High
Gauchers Disease 206 91.72 High High
Osteoporosis 6 88.08 High High
Neurologic Manifestations 6 79.96 Quite High
Pain 8 77.52 Quite High
Arrhythmia Under Development 2 71.64 Quite High
Death 4 65.60 Quite High
Deafness 4 64.20 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The secreted product was purified to apparent electrophoretic homogeneity using hydrophobic interaction chromatography and found to be produced in a fully glycosylated and a hypoglycosylated form, both of which cross-reacted with a human GBA-specific monoclonal antibody.
GBA Binding (cross-reacted) of
1) Confidence 0.37 Published 2006 Journal Biochem. Cell Biol. Section Abstract Doc Link 16609695 Disease Relevance 0.44 Pain Relevance 0.06
The majority of GBA mutations lead to the synthesis of GC with decreased catalytic function and/or stability.6 While it is assumed that disease severity depends on residual GC activity, this has been difficult to prove for most GBA mutations.7
GBA Binding (prove) of associated with disease
2) Confidence 0.32 Published 2010 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2909498 Disease Relevance 0.51 Pain Relevance 0
The establishment of the association between GBA mutations and the development of parkinsonian manifestations have brought new challenges for both the clinician and researchers.
GBA Binding (association) of associated with parkinson's disease
3) Confidence 0.31 Published 2010 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2909498 Disease Relevance 1.10 Pain Relevance 0
There are several lines of evidence that suggest there is an association between GBA mutations and development of Parkinson disease pathology.96,97 Although the risk of Parkinson disease is suggested to be increased, especially among individuals carrying “severe” GBA mutations, the penetrance and again the role of modifiers are not known for each GBA alteration.98 Furthermore, 99% of individuals carrying GBA mutations either in hetero- or homozygote states will not develop parkinsonian manifestations, limiting the genetic counseling even in “at risk” individuals in families with more than one person affected.
GBA Binding (association) of associated with parkinson's disease
4) Confidence 0.31 Published 2010 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2909498 Disease Relevance 1.04 Pain Relevance 0
Synchronized GBA in general is proposed to bind sensory events into one coherent conscious percept [12]–[16].
GBA Binding (bind) of
5) Confidence 0.30 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2754613 Disease Relevance 0.61 Pain Relevance 0.18

General Comments

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