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American Journal of Physiology. Cell Physiology|February 8, 2018
Branched fibers from old fast-twitch dystrophic muscles are the sites of terminal damage in muscular dystrophyLeonit Kiriaev, Sindy Kueh, John W Morley, et al.
Frontiers in Physiology|March 3, 2023
Six weeks of N-acetylcysteine antioxidant in drinking water decreases pathological fiber branching in MDX mouse dystrophic fast-twitch skeletal muscleAsma Redwan, Leonit Kiriaev, Sindy Kueh, et al.
American Journal of Physiology. Cell Physiology|August 25, 2021
Dystrophin-negative slow-twitch soleus muscles are not susceptible to eccentric contraction induced injury over the lifespan of the <i>mdx</i> mouseLeonit Kiriaev, Sindy Kueh, John W Morley, et al.
Frontiers in Physiology|July 22, 2021
Minocycline Treatment Reduces Mass and Force Output From Fast-Twitch Mouse Muscles and Inhibits Myosin Production in C2C12 MyotubesLeonit Kiriaev, Ben D Perry, David A Mahns, et al.
Plos Genetics|January 16, 2015
Altered Ca2+ kinetics associated with α-actinin-3 deficiency may explain positive selection for ACTN3 null allele in human evolutionStewart I Head, Stephen Chan, Peter J Houweling, et al.
Skeletal Muscle|June 22, 2022
Absence of the Z-disc protein α-actinin-3 impairs the mechanical stability of Actn3KO mouse fast-twitch muscle fibres without altering their contractile properties or twitch kineticsMichael Haug, Barbara Reischl, Stefanie Nübler, et al.
Bioarchitecture|June 29, 2013
Aged skeletal muscle retains the ability to fully regenerate functional architectureAntonio S J Lee, Judy E Anderson, Josephine E Joya, et al.
Nature Communications|February 1, 2017
Evidence for ACTN3 as a genetic modifier of Duchenne muscular dystrophyMarshall W Hogarth, Peter J Houweling, Kristen C Thomas, et al.
Human Molecular Genetics|December 19, 2015
Analysis of the ACTN3 heterozygous genotype suggests that α-actinin-3 controls sarcomeric composition and muscle function in a dose-dependent fashionMarshall W Hogarth, Fleur C Garton, Peter J Houweling, et al.
Human Molecular Genetics|May 4, 2011
Deficiency of α-actinin-3 is associated with increased susceptibility to contraction-induced damage and skeletal muscle remodelingJane T Seto, Monkol Lek, Kate G R Quinlan, et al.
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