Results 81 to 90 of about 7,107 (213)
Alternative splicing (AS) expands proteomic diversity and functional complexity in eukaryotes, regulated by spliceosomal components, RNA elements, and epigenetic modifications. Dysregulated AS contributes to diseases, including cancer, neurodegenerative disorders, and cardiovascular conditions, among others. Therapeutic interventions, such as antisense
Zhi‐Min Zhu +5 more
wiley +1 more source
Expression of the utrophin gene during myogenic differentiation [PDF]
The process of myogenic differentiation is known to be accompanied by large increases ( approximately 10-fold) in the expression of genes encoding cytoskeletal and membrane proteins including dystrophin and the acetylcholine receptor (AChR) subunits, via the effects of transcription factors belonging to the MyoD family.
A O, Gramolini, B J, Jasmin
openaire +2 more sources
Murine obscurin and Obsl1 have functionally redundant roles in sarcolemmal integrity, sarcoplasmic reticulum organization, and muscle metabolism. [PDF]
Biological roles of obscurin and its close homolog Obsl1 (obscurin-like 1) have been enigmatic. While obscurin is highly expressed in striated muscles, Obsl1 is found ubiquitously.
Blondelle, Jordan +13 more
core +1 more source
Modulation of PGC-1α activity as a treatment for metabolic and muscle-related diseases [PDF]
Physical inactivity is a predisposing factor for various disease states including obesity, cardiovascular disease, as well as for certain types of cancer. Regular endurance exercise mediates several beneficial effects such as increased energy expenditure
Handschin, Christoph +1 more
core +1 more source
Exploring Desmin as a Potential Modifier in Duchenne Muscular Dystrophy–Associated Cardiomyopathy
ABSTRACT Aim Duchenne muscular dystrophy (DMD), a rare X‐linked genetic disorder, is affecting skeletal and cardiac muscles due to the loss of the dystrophin protein. Modifier proteins, whose expression is altered in DMD patients, may influence disease progression.
Brice‐Emmanuel Guennec +12 more
wiley +1 more source
Molecular and Functional Analysis of the Utrophin Promoter [PDF]
Utrophin is a ubiquitously expressed cytoskeletal protein which is an important structural component of the mammalian neuromuscular junction. It shows extensive sequence similarity to dystrophin leading to postulation that utrophin may be able to compensate for the absence of dystrophin in Duchenne muscular dystrophy (DMD) patients.
C L, Dennis +3 more
openaire +2 more sources
Identification of new dystroglycan complexes in skeletal muscle. [PDF]
The dystroglycan complex contains the transmembrane protein β-dystroglycan and its interacting extracellular mucin-like protein α-dystroglycan. In skeletal muscle fibers, the dystroglycan complex plays an important structural role by linking the ...
Eric K Johnson +6 more
doaj +1 more source
Aryl Hydrocarbon Receptor in Health and Disease
Based on the structure and ligands of AhR, this review introduces the AhR‐related signaling pathways and their roles in health and diseases. Agonists and antagonists of AhR as well as new strategies for treatment using the microbial–AhR axis are summarized. A prospect was made for the future use of AhR as a therapeutic target.
Haonan Li +11 more
wiley +1 more source
Utrophin localization in normal and dystrophin-deficient heart. [PDF]
BACKGROUND The localization of dystrophin at the sarcolemma of cardiac skeletal fibers and cardiac Purkinje fibers has been described. Dystrophin deficiency produces clinical manifestations of disease in skeletal muscles and hearts of patients with Duchenne and Becker muscular dystrophy. Utrophin (or dystrophin-related protein),
Pons, Françoise +7 more
openaire +3 more sources
Visualization of actin filaments and monomers in somatic cell nuclei [PDF]
© The Author(s), 2013. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Molecular Biology of the Cell 24 (2013): 982-994, doi:10.1091/mbc.E12-09-0685.In addition to its long-
Belin, Brittany J. +3 more
core +1 more source

