S
Sabine Mai
Researcher at University of Manitoba
Publications - 201
Citations - 6230
Sabine Mai is an academic researcher from University of Manitoba. The author has contributed to research in topics: Telomere & Genome instability. The author has an hindex of 37, co-authored 191 publications receiving 5624 citations. Previous affiliations of Sabine Mai include Basel Institute for Immunology & University of Calgary.
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Journal ArticleDOI
Transient anomalous diffusion of telomeres in the nucleus of mammalian cells.
I. Bronstein,Yonatan Israel,Eldad Kepten,Sabine Mai,Yaron Shav-Tal,Eli Barkai,Yuval Garini,Yuval Garini +7 more
TL;DR: The transient diffusion is consistent with a model of telomeres that are subject to a local binding mechanism with a wide but finite distribution of waiting times and has important biological implications with respect to the genome organization in the nucleus.
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Tip60 is a haplo-insufficient tumour suppressor required for an oncogene-induced DNA damage response
Chiara Gorrini,Massimo Squatrito,Massimo Squatrito,Chiara Luise,Nelofer Syed,Daniele Perna,Landon Wark,Francesca Martinato,Domenico Sardella,Alessandro Verrecchia,Samantha Bennett,Stefano Confalonieri,Matteo Cesaroni,Francesco Marchesi,Milena Gasco,Eugenio Scanziani,Maria Capra,Sabine Mai,Paolo Nuciforo,Tim Crook,John Lough,Bruno Amati +21 more
TL;DR: In both mouse and human, Tip60 has a haplo-insufficient tumour suppressor activity that is independent from—but not contradictory with—its role within the ARF–p53 pathway.
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Fus deficiency in mice results in defective B-lymphocyte development and activation, high levels of chromosomal instability and perinatal death.
Geoff Hicks,Nagendra Singh,Nagendra Singh,Abudi Nashabi,Sabine Mai,G. Bozek,Ludger Klewes,D. Arapovic,E. K. White,Mark J. Koury,Eugene M. Oltz,L Van Kaer,L Van Kaer,H E Ruley +13 more
TL;DR: The results indicate that Fus is essential for viability of neonatal animals, influences lymphocyte development in a non-cell-intrinsic manner, has an intrinsic role in the proliferative responses of B cells to specific mitogenic stimuli and is required for the maintenance of genomic stability.
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Cyclin E amplification/overexpression is a mechanism of trastuzumab resistance in HER2+ breast cancer patients
Maurizio Scaltriti,Pieter Johan Adam Eichhorn,Javier Cortes,Ludmila Prudkin,Claudia Aura,Jose Jimenez,Sarat Chandarlapaty,Violeta Serra,Aleix Prat,Yasir H. Ibrahim,Marta Guzman,Magui Gili,Olga Graciela Cantu Rodriguez,Sonia Rodríguez,José Francisco Pérez,Simon Green,Sabine Mai,Neal Rosen,Clifford A. Hudis,José Baselga +19 more
TL;DR: The findings point to a causative role for cyclin E overexpression and the consequent increase inCDK2 activity in trastuzumab resistance and suggest that treatment with CDK2 inhibitors may be a valid strategy in patients with breast tumors with HER2 and Cyclin E coamplification/overexpression.
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Granzyme B (GraB) Autonomously Crosses the Cell Membrane and Perforin Initiates Apoptosis and GraB Nuclear Localization
TL;DR: It is concluded that GraB can enter cells autonomously but that perforin initiates the apoptotic process and the entry of GraB into the nucleus.