M
Ming Zhang
Researcher at University of Toronto
Publications - 73
Citations - 2443
Ming Zhang is an academic researcher from University of Toronto. The author has contributed to research in topics: DNA methylation & Amyotrophic lateral sclerosis. The author has an hindex of 26, co-authored 62 publications receiving 2055 citations. Previous affiliations of Ming Zhang include Chinese Academy of Sciences & Sunnybrook Health Sciences Centre.
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Journal ArticleDOI
The C9orf72 repeat size correlates with onset age of disease, DNA methylation and transcriptional downregulation of the promoter
Ilse Gijselinck,S. Van Mossevelde,J. van der Zee,Anne Sieben,Anne Sieben,Sebastiaan Engelborghs,J. De Bleecker,Adrian Ivanoiu,Olivier Deryck,Dieter Edbauer,Dieter Edbauer,Ming Zhang,Bavo Heeman,Veerle Bäumer,M Van den Broeck,Maria Mattheijssens,K. Peeters,Ekaterina Rogaeva,P. De Jonghe,Patrick Cras,Jean-Jacques Martin,P.P. De Deyn,Marc Cruts,C. Van Broeckhoven +23 more
TL;DR: It is shown that increased methylation of CpGs in the C9orf72 promoter may explain how an increasing G4C2 size lead to loss-of-function without excluding repeat length-dependent toxic gain- of-function.
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A meta-analysis of oxidative stress markers in schizophrenia
TL;DR: It was shown that TBARS and NO significantly increased in SCZ, while SOD activity significantly decreased in the disorganized type of SCZ patients, which demonstrated the involvement of oxidative stress in the pathophysiology of schizophrenia.
Journal ArticleDOI
Isoform-specific antibodies reveal distinct subcellular localizations of C9orf72 in amyotrophic lateral sclerosis.
Shangxi Xiao,Laura MacNair,Philip McGoldrick,Paul M. McKeever,Jesse R. McLean,Ming Zhang,Julia Keith,Lorne Zinman,Ekaterina Rogaeva,Janice Robertson +9 more
TL;DR: A noncoding hexanucleotide repeat expansion in C9orf72 is the most common cause of amyotrophic lateral sclerosis and frontotemporal lobar degeneration, and it has been reported that the repeat expansion causes a downregulation of C 9orf72 transcripts, suggesting that haploinsufficiency may contribute to disease pathogenesis.
Journal ArticleDOI
The C9orf72 repeat expansion itself is methylated in ALS and FTLD patients
Zhengrui Xi,Ming Zhang,Amalia C. Bruni,Raffaele Maletta,Rosanna Colao,Pietro Fratta,James M. Polke,Mary G. Sweeney,Ese E. Mudanohwo,Benedetta Nacmias,Sandro Sorbi,Maria Carmela Tartaglia,Innocenzo Rainero,Elisa Rubino,Lorenzo Pinessi,Daniela Galimberti,Ezequiel Surace,Philip McGoldrick,Paul M. McKeever,Danielle Moreno,Christine Sato,Yan Liang,Julia Keith,Lorne Zinman,Janice Robertson,Ekaterina Rogaeva +25 more
TL;DR: The results suggest that (G4C2)n-methylation might sometimes spread to the 5′-upstream region, but not vice versa, which may open up new perspectives for studying disease mechanisms, such as determining whether methylated and unmethylated repeats have the same ability to form a G-quadruplex configuration.
Journal ArticleDOI
A Predictive Metabolic Signature for the Transition From Gestational Diabetes Mellitus to Type 2 Diabetes
Amina Allalou,Amarnadh Nalla,Kacey J. Prentice,Ying Liu,Ming Zhang,Feihan F. Dai,Xian Ning,Lucy R. Osborne,Brian J. Cox,Erica P. Gunderson,Michael B. Wheeler +10 more
TL;DR: This study represents the first metabolomics study of the transition from GDM to T2D validated in an independent testing set, facilitating early interventions and predicted T1D incidence from a single fasting blood sample.