INT225793

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Context Info
Confidence 0.06
First Reported 2006
Last Reported 2006
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 1.77
Pain Relevance 0.06

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

transport (Ank) plasma membrane (Ank)
Anatomy Link Frequency
joints 2
Ank (Mus musculus)
Ppi-rs (Mus musculus)
Pain Link Frequency Relevance Heat
Osteoarthritis 30 57.76 Quite High
cytokine 6 5.00 Very Low Very Low Very Low
depression 4 5.00 Very Low Very Low Very Low
Inflammation 4 5.00 Very Low Very Low Very Low
adenocard 4 5.00 Very Low Very Low Very Low
spinal inflammation 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Calcification 92 96.84 Very High Very High Very High
Hyperostosis 2 93.80 High High
Syndrome 2 86.72 High High
Aging 26 77.64 Quite High
Osteoarthritis 30 57.76 Quite High
Parkinson's Disease 2 45.12 Quite Low
Disease 16 32.28 Quite Low
Osteoporosis 8 5.00 Very Low Very Low Very Low
Chondrocalcinosis 6 5.00 Very Low Very Low Very Low
Congenital Anomalies 6 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Both NPP1 deficient mice and mice homozygous for a natural C-terminal ANK mutant that appears to incapacitate ANK PPi transport function (ank/ank mice) spontaneously develop a progressive phenotype of pathologic soft tissue calcification that with increasing age comes to include perispinal ligament hyperostosis, periarticular calcification leading to ossific fusion of peripheral joints, extensive articular cartilage degeneration associated with HA deposits, and large artery calcification [22, 35].
ank Positive_regulation (incapacitate) of PPi in joints associated with calcification and hyperostosis
1) Confidence 0.06 Published 2006 Journal Purinergic Signal Section Body Doc Link PMC2254483 Disease Relevance 0.88 Pain Relevance 0.03
Both NPP1 deficient mice and mice homozygous for a natural C-terminal ANK mutant that appears to incapacitate ANK PPi transport function (ank/ank mice) spontaneously develop a progressive phenotype of pathologic soft tissue calcification that with increasing age comes to include perispinal ligament hyperostosis, periarticular calcification leading to ossific fusion of peripheral joints, extensive articular cartilage degeneration associated with HA deposits, and large artery calcification [22, 35].
ank Positive_regulation (incapacitate) of PPi in joints associated with calcification and hyperostosis
2) Confidence 0.06 Published 2006 Journal Purinergic Signal Section Body Doc Link PMC2254483 Disease Relevance 0.89 Pain Relevance 0.03

General Comments

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