INT312608

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.44
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.35
Pain Relevance 0

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

signal transduction (Musk) plasma membrane (Musk) kinase activity (Musk)
Musk (Mus musculus)
Pain Link Frequency Relevance Heat
anesthesia 1 15.20 Low Low
Action potential 1 5.00 Very Low Very Low Very Low
imagery 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Congenital Myasthenic Syndromes 22 100.00 Very High Very High Very High
Congenital Anomalies 2 96.16 Very High Very High Very High
Myasthenia Gravis 3 5.00 Very Low Very Low Very Low
Syndrome 3 5.00 Very Low Very Low Very Low
Respiratory Failure 2 5.00 Very Low Very Low Very Low
Muscle Weakness 2 5.00 Very Low Very Low Very Low
Frailty 1 5.00 Very Low Very Low Very Low
Ocular Toxicity (including Many Sub-types) 1 5.00 Very Low Very Low Very Low
Cognitive Disorder 1 5.00 Very Low Very Low Very Low
Disease 1 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Together, these findings suggest that impaired MuSK phosphorylation, which is a feature common to CMS due to MUSK and DOK7 mutations, is a key factor responsible for the abnormal endplate formation and presynaptic differentiation seen in CMS resulting from abnormalities of the agrin-MuSK signal transduction pathway.
Regulation (responsible) of Phosphorylation (phosphorylation) of MuSK associated with congenital myasthenic syndromes and congenital anomalies
1) Confidence 0.44 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2876883 Disease Relevance 0.35 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox