http://rdf.disgenet.org/resource/nanopub/NP535262.RAns0xc7TwGP75vtRFE00XQKtlQx4BK0YTOY4o9Lb5UVU
type: Nanopublication
created: 2016-05-13T12:45:47+02:00
rights: http://opendatacommons.org/licenses/odbl/1.0/
rights holder: IBIGroup
subject: SIO_000983
used data: disgenetv3.0rdf
authored by: http://orcid.org/0000-0001-5999-6269
authored by: http://orcid.org/0000-0002-7534-7661
authored by: 0000-0002-9383-528X
authored by: http://orcid.org/0000-0003-0169-8159
authored by: http://orcid.org/0000-0003-1244-7654
created by: http://orcid.org/0000-0003-0169-8159
version: v4.0.0.0

http://rdf.disgenet.org/resource/nanopub/NP535262.RAns0xc7TwGP75vtRFE00XQKtlQx4BK0YTOY4o9Lb5UVU130_assertion
type: Assertion
description: [The clinical relevance of maintaining a finely tuned balance between mitochondrial fusion and fission processes is underscored by the fact that the pathogenesis of certain hereditary neurodegenerative disorders such as autosomal dominant optic atrophy (ADOA) and Charcot-Marie-Tooth neuropathy type 2A (CMT2A) can now be linked to mutations in genes encoding mediators of mitochondrial fusion.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
evidence: DisGeNET evidence - LITERATURE
SIO_000772: http://identifiers.org/pubmed/16468021
was generated by: ECO_0000203

befree-2016
imported on: 2016-02-19

DisGeNET evidence - LITERATURE
type: ECO_0000212
comment: Gene-disease associations inferred from text-mining the literature.

disgenetv3.0rdf
version: v4.0.0