Results 121 to 130 of about 38,034 (262)

Time-dependent effect of Kinetin on C2C12 differentiation into myotubes.

open access: yes, 2021
C2C12 cells were grown in GM supplemented with DMSO (negative control) or with different concentrations of Kinetin at 0.1μM, 1μM and 10μM. Myog transcript levels and MCK activity was validated at 3 days (A and B), 5 days (C and D) and 7 days (E and F ...
Mark Isalan (26971)   +1 more
core   +1 more source

AGRN‐, LRP4‐, MUSK‐Related CMS: Clinical, Neurophysiological, Morphological, Genetic and Pathological Mechanisms

open access: yesMuscle &Nerve, EarlyView.
ABSTRACT Congenital myasthenic syndromes (CMS) are inherited disorders caused by mutations in genes encoding proteins essential for neuromuscular junction (NMJ) function. Pathogenic variants have been identified in more than 35 genes, underscoring the complexity of synaptic biology and the wide range of mechanisms that can compromise neuromuscular ...
Rocio‐Nur Villar‐Quiles   +5 more
wiley   +1 more source

MSCs influence C2C12 myoblast proliferation through paracrine mechanisms.

open access: yes, 2013
C2C12 cells were grown in single culture (C2C12) or exposed to MSC-derived CM (C2C12/MSC-CM) and their proliferative activity assessed by time lapse videomicroscopy (A-C), EdU (green) incorporation (D, E), Notch-1 and Hes-1 expression by RT-PCR (F ...
Chiara Sassoli (315671)   +9 more
core   +1 more source

Selective androgen receptor modulator, S42 has anabolic and anti-catabolic effects on cultured myotubes

open access: yesBiochemistry and Biophysics Reports, 2019
We previously identified a novel selective androgen receptor modulator, S42, that does not stimulate prostate growth but has a beneficial effect on lipid metabolism.
Yoshimi Muta   +8 more
doaj   +1 more source

The Differing Phenotypes of the Three Most Common Postsynaptic Congenital Myasthenic Syndromes Governed by Their Underlying Molecular Pathogenic Mechanisms

open access: yesMuscle &Nerve, EarlyView.
ABSTRACT The congenital myasthenic syndromes are rare disorders of impaired signal transmission at the neuromuscular junction. Despite next generation sequencing facilitating the identification of variants in myasthenic‐associated genes, these variants are frequently of unknown significance and the clinical diagnosis can be delayed.
David Beeson
wiley   +1 more source

Muscle‐Specific Kinase Signaling and Its Therapeutic Potential

open access: yesMuscle &Nerve, EarlyView.
ABSTRACT The function of the neuromuscular junction (NMJ) is compromised in many neuromuscular diseases (NMDs) such as autoimmune or congenital myasthenia gravis (MG), amyotrophic lateral sclerosis (ALS), spinal muscular atrophy (SMA), and muscular dystrophies.
Stine Marie Jensen   +2 more
wiley   +1 more source

Overexpression of survivin inhibited thimerosal-induced apoptosis in C2C12 myoblast cells.

open access: yes, 2013
A. C2C12-survivin with overexpression of survivin, C2C12-puro with control vector and normal C2C12 cells (Mock) were subjected to western blot analysis with antibody against survivin followed by densitometric quantification ...
Hua-Zhang Liu (300078)   +6 more
core   +1 more source

Autophagic flux data in differentiated C2C12 myotubes following exposure to acetylcholine and caffeine

open access: yesData in Brief, 2016
The C2C12 line of mouse myoblasts is a useful cell culture model in which to conduct in vitro analyses related to skeletal muscle. Here we present data regarding the autophagic response induced by two chemicals known to influence calcium release and ...
Darin Bloemberg, Joe Quadrilatero
doaj   +1 more source

Proteomic Profiling of Myofiber Repair Annexins and Their Role in Duchenne Muscular Dystrophy

open access: yesPROTEOMICS, EarlyView.
ABSTRACT Myofiber regeneration and membrane repair play crucial roles in maintaining the continuous physiological functioning of the neuromuscular system. A swift and efficient repair mechanism enables the rapid restoration of sarcolemmal integrity following cellular impairment in damaged skeletal muscles.
Paul Dowling   +6 more
wiley   +1 more source

Fn14 signalling participates in pristane‐induced murine lupus through exacerbating oxidative stress

open access: yesBritish Journal of Pharmacology, EarlyView.
Background and Purpose Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by oxidative stress and immune dysregulation. Fibroblast growth factor‐inducible 14 (Fn14) has been implicated in tissue injury, but its specific role in SLE pathogenesis remains unclear.
Zhu Yan   +8 more
wiley   +1 more source

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