INT142723

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Context Info
Confidence 0.38
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 4
Total Number 4
Disease Relevance 1.65
Pain Relevance 0.34

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

transferase activity, transferring glycosyl groups (A4GALT) Golgi apparatus (A4GALT) plasma membrane organization (A4GALT)
Anatomy Link Frequency
blood vessels 4
nerves 1
dorsal root ganglia 1
A4GALT (Homo sapiens)
Pain Link Frequency Relevance Heat
Potency 2 95.60 Very High Very High Very High
Bioavailability 1 88.48 High High
Lasting pain 3 83.28 Quite High
Pain 3 5.00 Very Low Very Low Very Low
Calcium channel 2 5.00 Very Low Very Low Very Low
palliative 1 5.00 Very Low Very Low Very Low
carbamazepine 1 5.00 Very Low Very Low Very Low
Analgesic 1 5.00 Very Low Very Low Very Low
Neuropathic pain 1 5.00 Very Low Very Low Very Low
Pain management 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Lysosomal Storage Diseases 3 99.78 Very High Very High Very High
Fabry Disease 34 98.70 Very High Very High Very High
Pain 7 83.28 Quite High
Targeted Disruption 2 73.36 Quite High
Coronary Heart Disease 4 71.92 Quite High
Stroke 6 70.32 Quite High
Disease 13 42.56 Quite Low
Lysosome Storage Disease 6 5.00 Very Low Very Low Very Low
Gauchers Disease 2 5.00 Very Low Very Low Very Low
Pompes Disease 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Fabry disease is an X-linked, hereditary, lysosomal storage disease caused by deficiency of the enzyme alpha-galactosidase A, which results in the accumulation of the neutral glycosphingolipid globotriaosylceramide (Gb3) in the walls of small blood vessels, nerves, dorsal root ganglia, renal glomerular and tubular epithelial cells, and cardiomyocytes.
Negative_regulation (deficiency) of Positive_regulation (accumulation) of Gb3 in blood vessels associated with lysosomal storage diseases and fabry disease
1) Confidence 0.38 Published 2007 Journal Ann. Intern. Med. Section Abstract Doc Link 17371887 Disease Relevance 0.50 Pain Relevance 0.08
Fabry disease is an X-linked, hereditary, lysosomal storage disease caused by deficiency of the enzyme alpha-galactosidase A, which results in the accumulation of the neutral glycosphingolipid globotriaosylceramide (Gb3) in the walls of small blood vessels, nerves, dorsal root ganglia, renal glomerular and tubular epithelial cells, and cardiomyocytes.
Negative_regulation (deficiency) of in nerves Positive_regulation (accumulation) of Gb3 in blood vessels associated with lysosomal storage diseases and fabry disease
2) Confidence 0.13 Published 2007 Journal Ann. Intern. Med. Section Abstract Doc Link 17371887 Disease Relevance 0.50 Pain Relevance 0.08
Fabry disease is an X-linked, hereditary, lysosomal storage disease caused by deficiency of the enzyme alpha-galactosidase A, which results in the accumulation of the neutral glycosphingolipid globotriaosylceramide (Gb3) in the walls of small blood vessels, nerves, dorsal root ganglia, renal glomerular and tubular epithelial cells, and cardiomyocytes.
Negative_regulation (deficiency) of in dorsal root ganglia Positive_regulation (accumulation) of Gb3 in blood vessels associated with lysosomal storage diseases and fabry disease
3) Confidence 0.13 Published 2007 Journal Ann. Intern. Med. Section Abstract Doc Link 17371887 Disease Relevance 0.50 Pain Relevance 0.08
Depending on the potency and selectivity of active compounds identified in the above processes, a probe can be defined if the potencies (IC50/EC50) of the identified agents are less than 1 ┬ÁM, and if they selectively act on GLA and effectively reduce Gb3 accumulation in patient cells.
Negative_regulation (reduce) of Positive_regulation (accumulation) of Gb3 associated with potency
4) Confidence 0.06 Published 2010 Journal Current Chemical Genomics Section Body Doc Link PMC2995157 Disease Relevance 0.15 Pain Relevance 0.09

General Comments

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