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Bernd Timmermann
Researcher at Max Planck Society
Publications - 161
Citations - 27435
Bernd Timmermann is an academic researcher from Max Planck Society. The author has contributed to research in topics: Gene & Genome. The author has an hindex of 45, co-authored 146 publications receiving 19299 citations. Previous affiliations of Bernd Timmermann include Max Delbrück Center for Molecular Medicine & University of Bergen.
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Journal ArticleDOI
LSD1 modulates the non-canonical integrin β3 signaling pathway in non-small cell lung carcinoma cells
Soyoung Lim,Iris Macheleidt,Priya Dalvi,Stephan C. Schäfer,Martin Kerick,Luka Ozretić,Sandra Ortiz-Cuaran,Julie George,Sabine Merkelbach-Bruse,Jürgen Wolf,Bernd Timmermann,Roman K. Thomas,Michal R. Schweiger,Reinhard Buettner,Margarete Odenthal +14 more
TL;DR: Findings point to a LSD1-integrin β3 axis, conferring attributes of invasiveness and tumor progression to lung adenocarcinoma.
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Transcriptomic and proteomic insight into the effects of a defined European mistletoe extract in Ewing sarcoma cells reveals cellular stress responses
M. Twardziok,M. Twardziok,M. Twardziok,David Meierhofer,Stefan T. Börno,Bernd Timmermann,S Jäger,Sengül Boral,Angelika Eggert,Catharina I. Delebinski,Georg Seifert +10 more
TL;DR: Since the combinatory extract viscumTT exerts highly effective pro-apoptotic effects on Ewing Sarcoma cells in vitro, this phytopolychemotherapy could be a promising adjuvant therapeutic option for paediatric patients with Ewing sarcoma.
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The cancer-associated U2AF35 470A>G (Q157R) mutation creates an in-frame alternative 5' splice site that impacts splicing regulation in Q157R patients.
TL;DR: Zhang et al. as mentioned in this paper found that the c.470A>G mutation not only leads to the Q157R substitution, but also creates an alternative 5' splice site (ss) resulting in the deletion of four amino acids (Q157Rdel).
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Low catalytic activity is insufficient to induce disease pathology in triosephosphate isomerase deficiency
Joanna Segal,Michael Mülleder,Michael Mülleder,Antje Krüger,Thure Adler,Manuela Scholze-Wittler,Lore Becker,Julia Calzada-Wack,Lillian Garrett,Sabine M. Hölter,Birgit Rathkolb,Jan Rozman,Ildiko Racz,Ralf Fischer,Dirk H. Busch,Frauke Neff,Martin Klingenspor,Thomas Klopstock,Nana-Maria Grüning,Steve Michel,Beata Lukaszewska‐McGreal,Ingo Voigt,Ludger Hartmann,Bernd Timmermann,Hans Lehrach,Eckhard Wolf,Wolfgang Wurst,Valerie Gailus-Durner,Helmut Fuchs,Martin Hrabě de Angelis,Heinrich Schrewe,Mariia Yuneva,Markus Ralser +32 more
TL;DR: A mouse model is generated in which exchange of a conserved catalytic amino acid residue reduces TPI specific activity without affecting the stability of the protein dimer, and a strong decline in TPI catalytic activity is not sufficient to explain the pathological onset of TPI deficiency.
Journal Article
Novel DNA sequence differences in the beta2-adrenergic receptor gene promoter region.
TL;DR: The structure, function, and mol