Published in Volume
111, Issue 6 (March 15, 2003)
J Clin Invest. 2003;111(6):925–925.
doi:10.1172/JCI16336C1.
Copyright ©
2003, The American Society for
Clinical Investigation.
Corrigendum
Idiopathic restrictive cardiomyopathy is part of the clinical
expression of cardiac troponin I mutations
Jens Mogensen1, Toru Kubo1,2, Mauricio Duque3, William Uribe3, Anthony Shaw1, Ross Murphy1, Juan R. Gimeno1, Perry Elliott1 and William J. McKenna1
1Department of Cardiological Sciences, St.
George’s Hospital Medical School, London, United Kingdom
2
Departamento de Cardiologia, Clinica Medellin, Medellin, Colombia
3
Department of Medicine and Geriatrics, Kochi Medical School, Japan
Published March 15, 2003
Original citation: J. Clin. Invest.
111:209–216 (2003). doi:10.1172/JCI16336.
Citation for this corrigendum: J. Clin. Invest.
111:925 (2003). doi:10.1172/JCI16336C1.
The authors wish to correct errors that appeared in the Methods section and throughout
the paper. The correct sentences are below. The authors regret the errors.
Mutation analysis of TNNI3 by direct sequencing identified a
87A→G nucleotide substitution of exon 8 resulting in an Asp190Gly amino acid
substitution that segregated with the disease in the family (maximal two-point lode
score: 4.8).
Direct sequencing of TNNI3 identified a 93G→A nucleotide
substitution of exon 8, which resulted in an Arg192His amino acid substitution.
