A
Anu Suomalainen
Researcher at University of Helsinki
Publications - 214
Citations - 19456
Anu Suomalainen is an academic researcher from University of Helsinki. The author has contributed to research in topics: Mitochondrial DNA & Mitochondrial disease. The author has an hindex of 67, co-authored 206 publications receiving 17041 citations. Previous affiliations of Anu Suomalainen include Montreal Neurological Institute and Hospital & University of Eastern Finland.
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Journal Article
A case of mitochondrial myopathy with MELAS-like features and polyneuropathy: ultrastructural and molecular studies.
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Genetic background of ataxia in children younger than 5 years in Finland
Erika Ignatius,Pirjo Isohanni,Max Pohjanpelto,Päivi Lahermo,Simo Ojanen,Virginia Brilhante,Eino Palin,Anu Suomalainen,Tuula Lönnqvist,Christopher J. Carroll,Christopher J. Carroll +10 more
TL;DR: There is a high heterogeneity of causative mutations in this cohort despite the defined age at onset, phenotypical overlap between patients, the founder effect, and genetic isolation in the Finnish population.
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Infantile SPASMS as presenting symptom of mitochondrial DNA 8993 T → G point mutation
Päivi Mäkelä-Bengs,Anu Suomalainen,Anna Majander,Juhani Rapola,Hannu Kalimo,Auli Nuutila,Helena Pihko +6 more
Journal Article
Abstract 1370: Overexpression of Mitochondria DNA Helicase, Twinkle, Ameliorates Cardiac Remodeling and Failure in Mice
Takahiro Inoue,Tomomi Ide,Henna Tyynismaa,Masayoshi Yoshida,Makoto Ando,Atsushi Tanaka,Koji Todaka,Dongchon Kang,Anu Suomalainen,Kenji Sunagawa +9 more
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Atomistic Molecular Dynamics Simulations of Mitochondrial DNA Polymerase γ: Novel Mechanisms of Function and Pathogenesis
Liliya Euro,Outi Haapanen,Tomasz Róg,Tomasz Róg,Ilpo Vattulainen,Ilpo Vattulainen,Anu Suomalainen,Vivek Sharma,Vivek Sharma +8 more
TL;DR: The first atomistic classical molecular dynamics simulations of the human Pol γ replicative complex show that DNA binding triggers remarkable changes in the enzyme structure, and indicate that noncatalytic mutations may disrupt replisomal interactions, thereby causingPol γ-associated neurodegenerative disorders.