Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy
DG Allen, NP Whitehead… - Physiological …, 2016 - journals.physiology.org
Dystrophin is a long rod-shaped protein that connects the subsarcolemmal cytoskeleton to a
complex of proteins in the surface membrane (dystrophin protein complex, DPC), with further …
complex of proteins in the surface membrane (dystrophin protein complex, DPC), with further …
Calcium sparks
H Cheng, WJ Lederer - Physiological reviews, 2008 - journals.physiology.org
The calcium ion (Ca2+) is the simplest and most versatile intracellular messenger known.
The discovery of Ca2+ sparks and a related family of elementary Ca2+ signaling events has …
The discovery of Ca2+ sparks and a related family of elementary Ca2+ signaling events has …
An injury-responsive Rac-to-Rho GTPase switch drives activation of muscle stem cells through rapid cytoskeletal remodeling
Many tissues harbor quiescent stem cells that are activated upon injury, subsequently
proliferating and differentiating to repair tissue damage. Mechanisms by which stem cells …
proliferating and differentiating to repair tissue damage. Mechanisms by which stem cells …
CRISPR-mediated genome editing restores dystrophin expression and function in mdx mice
Duchenne muscular dystrophy (DMD) is a degenerative muscle disease caused by genetic
mutations that lead to the disruption of dystrophin in muscle fibers. There is no curative …
mutations that lead to the disruption of dystrophin in muscle fibers. There is no curative …
Hypernitrosylated ryanodine receptor calcium release channels are leaky in dystrophic muscle
AM Bellinger, S Reiken, C Carlson, M Mongillo, X Liu… - Nature medicine, 2009 - nature.com
Duchenne muscular dystrophy is characterized by progressive muscle weakness and early
death resulting from dystrophin deficiency. Loss of dystrophin results in disruption of a large …
death resulting from dystrophin deficiency. Loss of dystrophin results in disruption of a large …
Microtubules underlie dysfunction in duchenne muscular dystrophy
RJ Khairallah, G Shi, F Sbrana, BL Prosser… - Science …, 2012 - science.org
Duchenne muscular dystrophy (DMD) is a fatal X-linked degenerative muscle disease
caused by the absence of the microtubule-associated protein dystrophin, which results in a …
caused by the absence of the microtubule-associated protein dystrophin, which results in a …
Calcium-induced calcium release in skeletal muscle
M Endo - Physiological reviews, 2009 - journals.physiology.org
Calcium-induced calcium release (CICR) was first discovered in skeletal muscle. CICR is
defined as Ca2+ release by the action of Ca2+ alone without the simultaneous action of …
defined as Ca2+ release by the action of Ca2+ alone without the simultaneous action of …
Calcium signaling in skeletal muscle development, maintenance and regeneration
MK Tu, JB Levin, AM Hamilton, LN Borodinsky - Cell calcium, 2016 - Elsevier
Skeletal muscle-specific stem cells are pivotal for tissue development and regeneration.
Muscle plasticity, inherent in these processes, is also essential for daily life activities. Great …
Muscle plasticity, inherent in these processes, is also essential for daily life activities. Great …
Remodeling of ryanodine receptor complex causes “leaky” channels: a molecular mechanism for decreased exercise capacity
AM Bellinger, S Reiken, M Dura… - Proceedings of the …, 2008 - National Acad Sciences
During exercise, defects in calcium (Ca2+) release have been proposed to impair muscle
function. Here, we show that during exercise in mice and humans, the major Ca2+ release …
function. Here, we show that during exercise in mice and humans, the major Ca2+ release …
Modulation of the ryanodine receptor and intracellular calcium
Abstract Ryanodine receptors (RyRs)/Ca2+ release channels, on the endoplasmic and
sarcoplasmic reticulum of most cell types, are required for intracellular Ca2+ release …
sarcoplasmic reticulum of most cell types, are required for intracellular Ca2+ release …