M
Michaela Yuen
Researcher at University of Sydney
Publications - 11
Citations - 382
Michaela Yuen is an academic researcher from University of Sydney. The author has contributed to research in topics: Actin & Nemaline myopathy. The author has an hindex of 7, co-authored 8 publications receiving 305 citations. Previous affiliations of Michaela Yuen include University of Amsterdam & Children's Hospital at Westmead.
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Journal ArticleDOI
Leiomodin-3 dysfunction results in thin filament disorganization and nemaline myopathy
Michaela Yuen,Sarah A. Sandaradura,James J. Dowling,James J. Dowling,Alla S. Kostyukova,Natalia Moroz,Kate G. R. Quinlan,Vilma Lotta Lehtokari,Gianina Ravenscroft,Emily J. Todd,Ozge Ceyhan-Birsoy,David S. Gokhin,Jérome Maluenda,Monkol Lek,Monkol Lek,Flora Nolent,Christopher T. Pappas,Stefanie M. Novak,Adele D'Amico,Edoardo Malfatti,Brett Thomas,Brett Thomas,Stacey Gabriel,Namrata Gupta,Mark J. Daly,Mark J. Daly,Biljana Ilkovski,Peter J. Houweling,Peter J. Houweling,Ann E. Davidson,Ann E. Davidson,Lindsay C. Swanson,Catherine A. Brownstein,Vandana Gupta,Livija Medne,Patrick Shannon,Nicole Martin,David P. Bick,Anders Flisberg,Eva Holmberg,Peter Van den Bergh,Pablo Lapunzina,Leigh B. Waddell,Darcée D. Sloboda,Enrico Bertini,David Chitayat,William R. Telfer,Annie Laquerrière,Carol C. Gregorio,Coen A.C. Ottenheijm,Carsten G. Bönnemann,Katarina Pelin,Alan H. Beggs,Yukiko K. Hayashi,Norma B. Romero,Nigel G. Laing,Ichizo Nishino,Carina Wallgren-Pettersson,Judith Melki,Velia M. Fowler,Daniel G. MacArthur,Daniel G. MacArthur,Kathryn N. North,Kathryn N. North,Kathryn N. North,Nigel F. Clarke +65 more
TL;DR: It is demonstrated that mutations in the gene encoding L MOD3 underlie congenital myopathy and demonstrate that LMOD3 is essential for the organization of sarcomeric thin filaments in skeletal muscle.
Journal ArticleDOI
Leiomodin-3 dysfunction results in thin filament disorganization and nemaline myopathy: corrigendum
Michaela Yuen,Sarah A. Sandaradura,James J. Dowling,Alla S. Kostyukova,Natalia Moroz,Kate G. R. Quinlan,Vilma-Lotta Lehtokari,Gianina Ravenscroft,Emily J. Todd,Ozge Ceyhan-Birsoy,David S. Gokhin,Jérome Maluenda,Monkol Lek,Flora Nolent,Christopher T. Pappas,Stefanie M. Novak,Adele D'Amico,Edoardo Malfatti,Brett Thomas,Stacey Gabriel,Namrata Gupta,Mark J. Daly,Biljana Ilkovski,Peter J. Houweling,Ann E. Davidson,Lindsay C. Swanson,Catherine A. Brownstein,Vandana Gupta,Livija Medne,Patrick Shannon,Nicole Martin,David P. Bick,Anders Flisberg,Eva Holmberg,Peter Van den Bergh,Pablo Lapunzina,Leigh B. Waddell,Darcée D. Sloboda,Enrico Bertini,David Chitayat,William R. Telfer,Annie Laquerrière,Carol C. Gregorio,Coen A.C. Ottenheijm,Carsten G. Bönnemann,Katarina Pelin,Alan H. Beggs,Yukiko K. Hayashi,Norma B. Romero,Nigel G. Laing,Ichizo Nishino,Carina Wallgren-Pettersson,Judith Melki,Velia M. Fowler,Daniel G. MacArthur,Kathryn N. North,Nigel F. Clarke +56 more
Journal ArticleDOI
Mutation-specific effects on thin filament length in thin filament myopathy
Josine M. de Winter,Barbara Joureau,Eun Jeong Lee,Balázs Kiss,Michaela Yuen,Vandana Gupta,Christopher T. Pappas,Carol C. Gregorio,Ger J.M. Stienen,Simon Edvardson,Carina Wallgren-Pettersson,Vilma Lotta Lehtokari,Katarina Pelin,Edoardo Malfatti,Norma B. Romero,Baziel G.M. van Engelen,Nicol C. Voermans,Sandra Donkervoort,Carsten G. Bönnemann,Nigel F. Clarke,Alan H. Beggs,Henk Granzier,Coen A.C. Ottenheijm +22 more
TL;DR: Thin filament myopathies are among the most common nondystrophic congenital muscular disorders, and are caused by mutations in genes encoding proteins related to skeletal muscle thin filament.
Journal ArticleDOI
Muscle weakness in TPM3-myopathy is due to reduced Ca2+-sensitivity and impaired acto-myosin cross-bridge cycling in slow fibres
Michaela Yuen,Michaela Yuen,Sandra T. Cooper,Steve Marston,Kristen J. Nowak,Elyshia McNamara,Nancy Mokbel,Biljana Ilkovski,Gianina Ravenscroft,John Rendu,Josine M. de Winter,Lars Klinge,Alan H. Beggs,Kathryn N. North,Coen A.C. Ottenheijm,Nigel F. Clarke +15 more
TL;DR: Weakness in TPM3-myopathy patients can be directly attributed to reduced slow fibre force at physiological [Ca(2+)], and impaired acto-myosin cross-bridge cycling kinetics, which suggests Ca(2+)-sensitizing drugs may represent a useful treatment for this condition.
Journal ArticleDOI
The Effects of Disease Models of Nuclear Actin Polymerization on the Nucleus
Leonid A. Serebryannyy,Michaela Yuen,Michaela Yuen,Megan Parilla,Sandra T. Cooper,Sandra T. Cooper,Primal de Lanerolle +6 more
TL;DR: The data suggest that nuclear actin filaments result in disruption of nuclear organization, which may contribute to the disease pathology.