Results 61 to 70 of about 8,048 (176)

Ubiquitylation by Trim32 causes coupled loss of desmin, Z-bands, and thin filaments in muscle atrophy [PDF]

open access: yes, 2013
During muscle atrophy, myofibrillar proteins are degraded in an ordered process in which MuRF1 catalyzes ubiquitylation of thick filament components (Cohen et al. 2009. J. Cell Biol. http://dx.doi.org/10.1083/jcb.200901052).
Cohen, Shenhav Orit   +3 more
core   +1 more source

A long non-coding RNA protects the heart from pathological hypertrophy [PDF]

open access: yes, 2014
The role of long noncoding RNA (lncRNA) in adult hearts is unknownalso unclear is how lncRNA modulates nucleosome remodeling. An estimated 70% of mouse genes undergo antisense transcription, including myosin heavy chain 7 (Myh7) that encodes molecular ...
Ashley, Euan   +18 more
core   +2 more sources

Small‐Molecule Targeting MuRF1 Protects Against Denervation‐Induced Diaphragmatic Dysfunction: Underlying Molecular Mechanisms

open access: yesJournal of Cachexia, Sarcopenia and Muscle, Volume 16, Issue 6, December 2025.
ABSTRACT Background Mechanical inactivity rapidly induces diaphragm muscle fibres' contractile dysfunction and atrophy. Diaphragm weakness can impair respiratory function, quality of life and increase risks of morbidity and mortality. Muscle RING‐finger protein‐1 (MuRF1) expression is upregulated during denervation and muscle inactivity and is known to
Fernando Ribeiro   +3 more
wiley   +1 more source

Coregulator-mediated control of skeletal muscle plasticity - A mini-review [PDF]

open access: yes, 2017
Skeletal muscle plasticity is a complex process entailing massive transcriptional programs. These changes are mediated by the action of nuclear receptors and other transcription factors. In addition, coregulator proteins have emerged as important players
Handschin, Christoph   +2 more
core   +1 more source

MYH7-related myopathies: clinical, histopathological and imaging findings in a cohort of Italian patients

open access: yesOrphanet Journal of Rare Diseases, 2016
BackgroundMyosin heavy chain 7 (MYH7)-related myopathies are emerging as an important group of muscle diseases of childhood and adulthood, with variable clinical and histopathological expression depending on the type and location of the mutation ...
C. Fiorillo   +38 more
semanticscholar   +1 more source

STIM1 Reduction Prevents Tubular Aggregate Formation and Compromises Muscle Performance in Ageing Mice

open access: yesJournal of Cachexia, Sarcopenia and Muscle, Volume 16, Issue 6, December 2025.
ABSTRACT Background Ageing is an irreversible process involving the gradual decline of cellular functions in all tissues. In male mice, age‐related loss of muscle force is accompanied by the formation of tubular aggregates, which are honeycomb‐like structures composed of membrane tubules, proteins and Ca2+ deposits. Tubular aggregates are also found in
Laura Pérez‐Guàrdia   +3 more
wiley   +1 more source

Congenital myopathies: an update

open access: yesDevelopmental Medicine & Child Neurology, 2019
Congenital myopathies comprise a clinical, histopathological, and genetic heterogeneous group of rare hereditary muscle diseases that are defined by architectural abnormalities in the muscle fibres.
K. Claeys
semanticscholar   +1 more source

Molecular genetics of cardiomyopathy: changing times, shifting paradigms [PDF]

open access: yes, 2003
The original publication is available at http://www.cvja.co.za/Includes bibliographyCongestive heart failure is a major problem in developed and developing countries alike.
Brink, Paul A.   +3 more
core  

Short-term, high-fat diet accelerates disuse atrophy and protein degradation in a muscle-specific manner in mice [PDF]

open access: yes, 2015
Background: A short-term high-fat diet impairs mitochondrial function and the ability of skeletal muscle to respond to growth stimuli, but it is unknown whether such a diet alters the ability to respond to atrophy signals. The purpose of this study was
Bollinger, Lance M   +6 more
core   +3 more sources

Functional phosphatome requirement for protein homeostasis, networked mitochondria, and sarcomere structure in C. elegans muscle [PDF]

open access: yes, 2017
Background: Skeletal muscle is central to locomotion and metabolic homeostasis. The laboratory worm C. elegans has been developed into a genomic model for assessing the genes and signals that regulate muscle development and protein degradation. Past work
Alessi   +59 more
core   +1 more source

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