F
Felix T. Wieland
Researcher at Heidelberg University
Publications - 158
Citations - 22192
Felix T. Wieland is an academic researcher from Heidelberg University. The author has contributed to research in topics: COPI & Golgi apparatus. The author has an hindex of 71, co-authored 158 publications receiving 20604 citations. Previous affiliations of Felix T. Wieland include Stanford University.
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Brefeldin A-induced increase of sphingomyelin synthesis. Assay for the action of the antibiotic in mammalian cells.
TL;DR: Using a radioactively labeled truncated ceramide this increase in sphingomyelin synthesis is easily detectable, and thus this method can serve as a convenient biochemical assay for the action of brefeldin A in mammalian cells.
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ArfGAP1 activity and COPI vesicle biogenesis.
TL;DR: It is found that catalytic amounts of Arf1GAP1 significantly reduce the yield of purified COPI vesicles and that Arf 1 rather than ArfGAP 1 constitutes a stoichiometric component of the COPI coat.
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Identification of novel sphingolipid-binding motifs in mammalian membrane proteins
Patrik Björkholm,Andreas M. Ernst,Moritz Hacke,Felix T. Wieland,Britta Brügger,Gunnar von Heijne +5 more
TL;DR: The ability of the motif-containing candidate proteins to bind sphingolipids with high specificity opens new perspectives on their respective regulation and function.
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Induction of cortical endoplasmic reticulum by dimerization of a coatomer-binding peptide anchored to endoplasmic reticulum membranes.
Grégory Lavieu,Lelio Orci,Lei Shi,Michael Geiling,Mariella Ravazzola,Felix T. Wieland,Pierre Cosson,James E. Rothman +7 more
TL;DR: It is suggested that Ist2 dimerization triggers coatomer binding and clustering of this protein into domains that traffic at the microtubule growing plus-end to generate the cER beneath the plasma membrane.
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Tumor-specific silencing of COPZ2 gene encoding coatomer protein complex subunit ζ2 renders tumor cells dependent on its paralogous gene COPZ1
Michael Shtutman,Mirza S. Baig,Elina Levina,Gregory Hurteau,Chang-uk Lim,Eugenia V. Broude,Mikhail A. Nikiforov,Timothy T. Harkins,C. Steven Carmack,Ye Ding,Felix T. Wieland,Ralph Buttyan,Igor B. Roninson +12 more
TL;DR: Silencing of microRNA 152 in different cancers and the ensuing down-regulation of its host gene COPZ2 offer a therapeutic opportunity for proliferation-independent selective killing of tumor cells by COPZ1-targeting agents.