ArticleJAMA neurology2018
Interpreting Genetic Variants in Titin in Patients With Muscle Disorders.
Article in JAMA neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 92 citations in OpenAlex.
- Poly(A)+ selection limits detection of long and alternatively spliced transcripts compared with rRNA depletion in RNA-Sequencing.BMC genomics · 2026Article
- A comprehensive framework for the interpretation of TTN missense variants.Genome medicine · 2026Article
- Epidemiological report and diagnostic approach used in the neuromuscular population of Liege, Belgium.Orphanet journal of rare diseases · 2025Article
- Titinopathies: Phenotype - genotype heterogeneity in an Indian cohort.Journal of neuromuscular diseases · 2025Article
- Analysis ofCirculation. Genomic and precision medicine · 2025Article
- Congenital Titinopathy: Comprehensive Characterization of the Most Severe End of the Disease Spectrum.Annals of neurology · 2025Article
- Pathomechanisms of Monoallelic variants in TTN causing skeletal muscle disease.Human molecular genetics · 2024Article
- Reanalysis of RNA sequencing data ends diagnostic odyssey and expands the phenotypic spectrum of congenital titinopathy.American journal of medical genetics. Part A · 2024Article
- Taking on the Titin: Muscle imaging as a diagnostic marker of biallelicJournal of neuromuscular diseases · 2024Article
- Inferring disease course from differential exon usage in the wide titinopathy spectrum.Annals of clinical and translational neurology · 2024Article
- A Titin Truncating Variant Causing a Dominant Myopathy With Cardiac Involvement in a Large Family: The Exception That Proves the Rule.Neurology. Genetics · 2024Article
- Prenatal Diagnosis of Fryns Syndrome through Identification of Two Novel Splice Variants in theLife (Basel, Switzerland) · 2024Article
- Article
- Titin copy number variations associated with dominant inherited phenotypes.Journal of medical genetics · 2024Article
- Digenic inheritance involving a muscle-specific protein kinase and the giant titin protein causes a skeletal muscle myopathy.Nature genetics · 2024Article
- Genetic Determinants of Atherogenic Indexes.Genes · 2023Article
- Fetal akinesia deformation sequence syndrome associated with recessive TTN variants.American journal of medical genetics. Part A · 2023Article
- Use of animal models to understand titin physiology and pathology.Journal of cellular and molecular medicine · 2022Review
- Article
- Identification and characterization of extrachromosomal circular DNA in alcohol induced osteonecrosis of femoral head.Frontiers in genetics · 2022Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
41 authors at 17 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Importance: Mutations in the titin gene (TTN) cause a wide spectrum of genetic diseases. The interpretation of the numerous rare variants identified in TTN is a difficult challenge given its large size. Objective: To identify genetic variants in titin in a cohort of patients with muscle disorders. Design, Setting, and Participants: In this case series, 9 patients with titinopathy and 4 other patients with possibly disease-causing variants in TTN were identified. Titin mutations were detected through targeted resequencing performed on DNA from 504 patients with muscular dystrophy, congenital myopathy, or other skeletal muscle disorders. Patients were enrolled from 10 clinical centers in April 2012 to December 2013. All of them had not received a diagnosis after undergoing an extensive investigation, including Sanger sequencing of candidate genes. The data analysis was performed between September 2013 and January 2017. Sequencing data were analyzed using an internal custom bioinformatics pipeline. Main Outcomes and Measures: The identification of novel mutations in the TTN gene and novel patients with titinopathy. We performed an evaluation of putative causative variants in the TTN gene, combining genetic, clinical, and imaging data with messenger RNA and/or protein studies. Results: Of the 9 novel patients with titinopathy, 5 (55.5%) were men and the mean (SD) age at onset was 25 (15.8) years (range, 0-46 years). Of the 4 other patients (3 men and 1 woman) with possibly disease-causing TTN variants, 2 (50%) had a congenital myopathy and 2 (50%) had a slowly progressive distal myopathy with onset in the second decade. Most of the identified mutations were previously unreported. However, all the variants, even the already described mutations, require careful clinical and molecular evaluation of probands and relatives. Heterozygous truncating variants or unique missense changes are not sufficient to make a diagnosis of titinopathy. Conclusions and Relevance: The interpretation of TTN variants often requires further analyses, including a comprehensive evaluation of the clinical phenotype (deep phenotyping) as well as messenger RNA and protein studies. We propose a specific workflow for the clinical interpretation of genetic findings in titin.
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