Results 101 to 110 of about 22,741 (230)

Acute exercise modifies titin phosphorylation and increases cardiac myofilament stiffness

open access: yesFrontiers in Physiology, 2014
Titin-based myofilament stiffness is largely modulated by phosphorylation of its elastic I-band regions N2-Bus (decreases passive stiffness, PT) and PEVK (increases PT). Here, we tested the hypothesis that acute exercise changes titin phosphorylation and
Anna Eliane Müller   +6 more
doaj   +1 more source

Clash of the titin

open access: yesThe Journal of Cell Biology, 2002
![Graphic][1] Sarcomere thick filaments (white) are disrupted by inhibition of titin–MURF-1 binding (right). The sarcomere is more than a complicated piece of structural machinery. According to new results by McElhinny et al.
openaire   +2 more sources

Autoantibodies in Patients With Arrhythmogenic Cardiomyopathy Activate GSK‐3β, Resulting in a Loss of Cardiomyocyte Cohesion

open access: yesActa Physiologica, Volume 242, Issue 7, July 2026.
ABSTRACT Background Arrhythmogenic cardiomyopathy (ACM) is an inherited cardiac desmosome disease, as more than 50% of affected patients carry pathogenic variants in desmosome protein‐coding genes. In this study, we focused on the role and mechanisms of pathogenic and non‐pathogenic autoantibodies against intercalated disc (ICD) proteins such as ...
Soumyata Pathak   +15 more
wiley   +1 more source

Increased titin compliance reduced length-dependent contractionand slowed cross-bridge kinetics in skinned myocardial strips from Rbm20ΔRRM mice

open access: yesFrontiers in Physiology, 2016
Titin is a giant protein spanning from the Z-disk to the M-band of the cardiac sarcomere. In the I-band titin acts as a molecular spring, contributing to passive mechanical characteristics of the myocardium throughout a heartbeat.
Hannah C. Pulcastro   +6 more
doaj   +1 more source

The role of titin in muscular disorders

open access: yesAnnals of Medicine, 2003
Titin, the biggest single (poly) peptide found in humans, and throughout nature so far, was long considered as a good candidate for inherited muscle diseases. However, disease-causing defects were not known until recently, when this central sarcomeric protein was associated with human skeletal tibial muscular dystrophy (TMD/LGMD2J), dilated ...
J Peter V, Hackman   +2 more
openaire   +2 more sources

The Molecular Diagnosis of Myopathies: Integrating Genomic, Proteomic, and Pathological Insights Toward Precision Medicine

open access: yesClinical Genetics, Volume 110, Issue 1, Page 15-28, July 2026.
Advances in genomic, proteomic, and transcriptomic technologies are transforming the diagnosis of genetic myopathies. When integrated with traditional muscle pathology, multi‐omics approaches improve diagnostic yield, clarify disease mechanisms, and support more precise, mechanism‐based therapeutic strategies for patients with neuromuscular disorders ...
Ludmila Alem   +2 more
wiley   +1 more source

Table_1_Urinary Titin Is Increased in Patients After Cardiac Surgery.XLSX [PDF]

open access: yes, 2019
Background: Few non-invasive biomarkers have been used to detect myocardial injury in patients with heart diseases. Recently, the N-terminal fragment (N-titin) of titin, a giant sarcomeric protein, which is involved in muscular passive tension and ...
Naritomo Nishioka (6313406)   +4 more
core   +1 more source

Perturbation of the titin/MURF1 signaling complex is associated with hypertrophic cardiomyopathy in a fish model and in human patients

open access: yesDisease Models & Mechanisms, 2019
Hypertrophic cardiomyopathy (HCM) is a hereditary disease characterized by cardiac hypertrophy with diastolic dysfunction. Gene mutations causing HCM have been found in about half of HCM patients, while the genetic etiology and pathogenesis remain ...
Yuta Higashikuse   +15 more
doaj   +1 more source

Distal Agrin (AGRN) Congenital Myasthenic Syndrome With Mitochondrial Dysfunction

open access: yesEuropean Journal of Neurology, Volume 33, Issue 7, July 2026.
ABSTRACT Background Agrin‐congenital myasthenic syndrome (AGRN‐CMS) is a rare, heterogeneous genetic disorder of the neuromuscular transmission that can present from infancy to adulthood. The clinical phenotype includes distal weakness mimicking distal myopathies.
Mariana Manoel Oku   +4 more
wiley   +1 more source

Actin-titin interaction in cardiac myofibrils: Probing a physiological role [PDF]

open access: yes, 1997
Linke WA, Ivemeyer M, Labeit S, Hinssen H, Ruegg JC, Gautel M. Actin-titin interaction in cardiac myofibrils: Probing a physiological role. BIOPHYSICAL JOURNAL.
Labeit, S   +11 more
core   +1 more source

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