INT296937

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Context Info
Confidence 0.73
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.63
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.

cytoskeletal protein binding (TPM1) cytosol (TPM1) cytoskeleton (TPM1)
cytoskeleton organization (TPM1) cytoplasm (TPM1)
TPM1 (Homo sapiens)
Pain Link Frequency Relevance Heat
fibrosis 1 5.00 Very Low Very Low Very Low
anesthesia 1 5.00 Very Low Very Low Very Low
adenocard 1 5.00 Very Low Very Low Very Low
Action potential 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Nemaline Myopathy 30 93.24 High High
Disease 3 91.52 High High
Muscle Weakness 5 58.04 Quite High
Muscle Disease 5 45.56 Quite Low
Acquired Immune Deficiency Syndrome Or Hiv Infection 3 42.32 Quite Low
Infection 1 42.00 Quite Low
Frailty 4 33.04 Quite Low
Respiratory Failure 8 9.00 Low Low
Muscle Hypotonia 10 7.04 Low Low
Fibrosis 1 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
-tropomyosin (TPM2),23 and troponin T1 (TNNT1).24 Genes for these proteins have been localized and mutations are fully characterized.11,25 Nebulin gene mutations are seen most commonly in autosomal recessive cases and these patients present as typical congenital NM.21 Some authors demonstrated with linkage studies that nebulin gene mutations at 2q21.2-q22 are responsible for 50% of the cases of NM.21 TPM3 mutations have been described in rare cases of dominant and recessive cases of NM, and rarely are TPM2 and TNNT1 also implicated.20 ACTA1 mutations at 1q42 are reported to comprise 10% of the cases of NM,22 and are more common in severe cases of NM.1
Localization (localized) of tropomyosin associated with nemaline myopathy
1) Confidence 0.73 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2824868 Disease Relevance 0.63 Pain Relevance 0

General Comments

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