R
Ralph Tiedt
Researcher at University Hospital of Basel
Publications - 15
Citations - 5346
Ralph Tiedt is an academic researcher from University Hospital of Basel. The author has contributed to research in topics: Transgene & Genetically modified mouse. The author has an hindex of 10, co-authored 12 publications receiving 5015 citations. Previous affiliations of Ralph Tiedt include University of Basel & University of Pavia.
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Journal ArticleDOI
A Gain-of-Function Mutation of JAK2 in Myeloproliferative Disorders
Robert Kralovics,Francesco Passamonti,Andreas Buser,Soon Siong Teo,Ralph Tiedt,Jakob Passweg,André Tichelli,Mario Cazzola,Radek C. Skoda +8 more
TL;DR: Genetic evidence and in vitro functional studies indicate that V617F gives hematopoietic precursors proliferative and survival advantages and a high proportion of patients with myeloproliferative disorders carry a dominant gain-of-function mutation of JAK2.
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Ratio of mutant JAK2-V617F to wild-type Jak2 determines the MPD phenotypes in transgenic mice
Ralph Tiedt,Hui Hao-Shen,Marta Anna Sobas,Marta Anna Sobas,Renate Looser,Stephan Dirnhofer,Jürg Schwaller,Radek C. Skoda +7 more
TL;DR: Higher levels of JAK2-V617F in mouse bone marrow by retroviral transduction caused a PV-like phenotype without thrombocytosis, consistent with the hypothesis that the ratio of mutant to wild-type JAK1 is critical for the phenotypic manifestation.
Journal Article
Ratio of mutant JAK2-V617F to wild-type Jak2 determines the MPD phenotypes in transgenic mice. Commentary
Ross L. Levine,Ralph Tiedt,Hui Hao-Shen,Marta Anna Sobas,Renate Looser,Stephan Dirnhofer,Jürg Schwaller,Radek C. Skoda +7 more
TL;DR: In this article, the authors generated JAK2-V617F transgenic mice with the sequences encoding the kinase domain placed in the inverse orientation and flanked by antiparallel loxP sites.
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Pf4-Cre transgenic mice allow the generation of lineage-restricted gene knockouts for studying megakaryocyte and platelet function in vivo
TL;DR: To generate transgenic mice that express Cre-recombinase exclusively in the megakaryocytic lineage, a mouse bacterial artificial chromosome clone is modified and the first exon of the platelet factor 4 (Pf4), also called CXCL4, is replaced with a codon-improved Cre cDNA.
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Talin is required for integrin-mediated platelet function in hemostasis and thrombosis
Brian G. Petrich,Patrizia Marchese,Zaverio M. Ruggeri,Saskia Spiess,Rachel M. Weichert,Feng Ye,Ralph Tiedt,Radek C. Skoda,Susan J. Monkley,David R. Critchley,Mark H. Ginsberg +10 more
TL;DR: It is established that platelet talin plays a crucial role in hemostasis and provided the first proof that talin is required for the activation and function of mammalian α2β1 and αIIbβ3 integrins in vivo.