Editorial [Welcome to our Recent Patents on Biotechnology Special Edition on Skeletal Muscle Diseases!]

2012 ◽  
Vol 6 (3) ◽  
pp. 155-156 ◽  
Author(s):  
Marco Brotto
Keyword(s):  
Skeletal Muscle ◽  
Special Edition ◽  
Muscle Diseases

Tropomyosin mutations responsible for muscle weakness in inherited skeletal muscle diseases

2008 ◽  
pp. 20-21
Author(s):  
Julien Ochala ◽  
Anders Oldfors ◽  
Lars Larsson
Keyword(s):  
Skeletal Muscle ◽  
Muscle Weakness ◽  
Muscle Diseases

scholarly journals Calsequestrin: a well-known but curious protein in skeletal muscle

2020 ◽  
Vol 52 (12) ◽  
pp. 1908-1925
Author(s):  
Jin Seok Woo ◽  
Seung Yeon Jeong ◽  
Ji Hee Park ◽  
Jun Hee Choi ◽  
Eun Hui Lee
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Human Skeletal Muscle ◽  
Rabbit Skeletal Muscle ◽  
Muscle Type ◽  
Muscle Diseases ◽  
The Past ◽  
Muscle Tissues ◽  
Suitable Amount ◽  
Terminal Cisternae

AbstractCalsequestrin (CASQ) was discovered in rabbit skeletal muscle tissues in 1971 and has been considered simply a passive Ca2+-buffering protein in the sarcoplasmic reticulum (SR) that provides Ca2+ ions for various Ca2+ signals. For the past three decades, physiologists, biochemists, and structural biologists have examined the roles of the skeletal muscle type of CASQ (CASQ1) in skeletal muscle and revealed that CASQ1 has various important functions as (1) a major Ca2+-buffering protein to maintain the SR with a suitable amount of Ca2+ at each moment, (2) a dynamic Ca2+ sensor in the SR that regulates Ca2+ release from the SR to the cytosol, (3) a structural regulator for the proper formation of terminal cisternae, (4) a reverse-directional regulator of extracellular Ca2+ entries, and (5) a cause of human skeletal muscle diseases. This review is focused on understanding these functions of CASQ1 in the physiological or pathophysiological status of skeletal muscle.

Recapitulating pathophysiology of skeletal muscle diseases in vitro using primary mouse myoblasts on a nanofibrous platform

2021 ◽  
Vol 32 ◽  
pp. 102341
Author(s):  
Aditi Jain ◽  
Manisha Behera ◽  
Venkatraman Ravi ◽  
Sneha Mishra ◽  
Nagalingam R. Sundaresan ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Diseases ◽  
Primary Mouse

scholarly journals Microtubules that form the stationary lattice of muscle fibers are dynamic and nucleated at Golgi elements

2013 ◽  
Vol 203 (2) ◽  
pp. 205-213 ◽  
Author(s):  
Sarah Oddoux ◽  
Kristien J. Zaal ◽  
Victoria Tate ◽  
Aster Kenea ◽  
Shuktika A. Nandkeolyar ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Mouse Muscle ◽  
Muscle Diseases ◽  
Superresolution Microscopy ◽  
Nuclear Membranes ◽  
Organizing Center ◽  
Static Images

Skeletal muscle microtubules (MTs) form a nonclassic grid-like network, which has so far been documented in static images only. We have now observed and analyzed dynamics of GFP constructs of MT and Golgi markers in single live fibers and in the whole mouse muscle in vivo. Using confocal, intravital, and superresolution microscopy, we find that muscle MTs are dynamic, growing at the typical speed of ∼9 µm/min, and forming small bundles that build a durable network. We also show that static Golgi elements, associated with the MT-organizing center proteins γ-tubulin and pericentrin, are major sites of muscle MT nucleation, in addition to the previously identified sites (i.e., nuclear membranes). These data give us a framework for understanding how muscle MTs organize and how they contribute to the pathology of muscle diseases such as Duchenne muscular dystrophy.

scholarly journals NF-κB signaling in skeletal muscle: prospects for intervention in muscle diseases

2008 ◽  
Vol 86 (7) ◽  
pp. 747-759 ◽  
Author(s):  
Foteini Mourkioti ◽  
Nadia Rosenthal
Keyword(s):  
Skeletal Muscle ◽  
Muscle Diseases
Sign in / Sign up

Export Citation Format

Share Document