Results 1 to 10 of about 26,024 (216)

Immunological and Structural Characterization of Titin Main Immunogenic Region; I110 Domain Is the Target of Titin Antibodies in Myasthenia Gravis

open access: yesBiomedicines, 2023
Myasthenia gravis (MG) is an autoimmune disease caused by antibodies targeting the neuromuscular junction (NJ) of skeletal muscles. The major MG autoantigen is nicotinic acetylcholine receptor.
Christos Stergiou   +13 more
doaj   +5 more sources

Cardiac Titin [PDF]

open access: yesCirculation, 2010
Titin constitutes the third myofilament of cardiac muscle, with a single giant polypeptide spanning from Z-disk to the M-band region of the sarcomere1 (Fig. 1). The ∼1.0 MDa region in the I-band is extensible and consists of tandemly arranged immunoglobulin (Ig)-like domains that make up proximal (near Z-disk) and distal (near A-I junction) segments ...
Henk L Granzier, Martin LeWinter
exaly   +3 more sources

Urinary Proteome Profiling by Several Methods Identifies Titin as the Most-Differentiating Noninvasive Urinary Biomarker of Disease Severity in Becker Muscular Dystrophy [PDF]

open access: yesProteomes
Background: Beckers muscular dystrophy (BMD) is a clinically heterogeneous dystrophinopathy caused by in-frame mutations in the dystrophin gene, resulting in variable disease severity.
Kimchi K. Le   +7 more
doaj   +2 more sources

Titin modulation and left ventricular remodelling in chronic primary mitral regurgitation [PDF]

open access: yesFrontiers in Cardiovascular Medicine
BackgroundLeft ventricular (LV) remodelling in mitral valve prolapse (MVP) is usually induced by chronic mitral regurgitation (MR), however it can also be disproportionate to the volume load, generating the hypothesis of MVP cardiomyopathy.
Lobke L. Pype   +19 more
doaj   +2 more sources

The titin N2A-MARP signalosome constrains muscle longitudinal hypertrophy in response to stretch [PDF]

open access: yeseLife
Titin-based mechanosensing is a key driver of trophic signaling in muscle, yet the downstream pathways linking titin sensing to muscle remodeling remain poorly understood.
Robbert van der Pijl   +12 more
doaj   +2 more sources

Association between empagliflozin exposure and skeletal muscle degeneration in patients with heart failure [PDF]

open access: yesBMC Cardiovascular Disorders
Background Sodium–glucose co-transporter 2 inhibitors (SGLT2i) have become essential in the management of heart failure. Their prognostic benefits are consistent across older adults, frail, and underweight patients, but there may be potential adverse ...
Tatsuya Nishikawa   +23 more
doaj   +2 more sources

Anti-titin antibody is associated with more frequent hospitalization to manage thymoma-associated myasthenia gravis

open access: yesFrontiers in Neurology, 2022
Background and purposeAnti-titin antibodies are antistriational antibodies associated with thymoma-associated myasthenia gravis (MG). We evaluated whether the patients with anti-titin antibody are more frequently hospitalized to manage thymoma-associated
Ki Hoon Kim   +4 more
doaj   +1 more source

E3-ligase knock down revealed differential titin degradation by autopagy and the ubiquitin proteasome system

open access: yesScientific Reports, 2021
The sarcomere protein titin is a major determinant of cardiomyocyte stiffness and ventricular distensibility. The constant mechanical stress on titin requires well-controlled protein quality control, the exact mechanisms of which have not yet been fully ...
Erik Müller   +5 more
doaj   +1 more source

Protein Quality Control at the Sarcomere: Titin Protection and Turnover and Implications for Disease Development

open access: yesFrontiers in Physiology, 2022
Sarcomeres are mainly composed of filament and signaling proteins and are the smallest molecular units of muscle contraction and relaxation. The sarcomere protein titin serves as a molecular spring whose stiffness mediates myofilament extensibility in ...
Sebastian Kötter, Martina Krüger
doaj   +1 more source

Titin [PDF]

open access: yesCirculation, 2001
Studies by Frank, Starling, and colleagues demonstrated that elevations of end-diastolic volume increase cardiac output in working hearts,1 a phenomenon referred to as the Frank-Starling (FS) relationship. It stands as one of earliest descriptions of the importance of diastolic dimensions to systolic function, yet how alterations in sarcomere length ...
John L. Sutko   +2 more
openaire   +1 more source

Home - About - Disclaimer - Privacy