http://rdf.disgenet.org/resource/nanopub/NP634890.RASfuX3rU2W37Rn0ayPw2TdKeer8I7G_otkEDr2DQ3bSg
type: Nanopublication
created: 2016-05-13T12:46:33+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/NP634890.RASfuX3rU2W37Rn0ayPw2TdKeer8I7G_otkEDr2DQ3bSg130_assertion
type: Assertion
description: [To assess whether this functional phenomenon was a direct result of altered Ca(2+) affinity or was caused by altered troponin-tropomyosin switching, we assessed Ca(2+) binding of the regulatory site of cardiac troponin C in wild-type or mutant troponin complex and thin filaments using a fluorescent probe (2-[4'-{iodoacetamido}aniline]-naphthalene-6-sulfonate) attached to Cys35 of cardiac troponin C. The Ca(2+)-binding affinity (pCa(50)=6.57+/-0.03) of reconstituted troponin complex was unaffected by all of the HCM and dilated cardiomyopathy troponin mutants tested, with the exception of the troponin I Arg145Gly HCM mutation, which caused an increase (DeltapCa(50)=+0.31+/-0.05).]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine.
evidence: DisGeNET evidence - LITERATURE
SIO_000772: http://identifiers.org/pubmed/17932326
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